Objective To investigate the effects of propofol on nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) levels in blood and lung during endotoxic shock in rats.Methods Seventy-two male Wistar rats weighing 180-220 g were randomly divided into thiee groups :group Ⅰ control (C) ( n = 8) ; group Ⅱ endotoxic shock (L) ( n = 32) and group Ⅲ propofol + endotoxic shock (P) ( n = 32) . The animals were anesthetized with 3% pentobarbital 25 mg?kg-1 , tracheostomized and mechanically ventilated . Carotid and pulmonary artery were cannulated for MAP and MPAP monitoring. In group Ⅱ (L) and Ⅲ (P) endotoxin 10 mg?kg-1 was injected intraperitoneally. In group P 10 min before endotoxin administration subcutaneous propofol infusion was started at a rate of 20 mg?kg-1?h-1 . In control group normal saline(NS) was given ip instead of endotoxin. Venous blood samples were taken at 30, 90, 180 and 360 min after intraperitoneal endotoxin or NS injection. In group L and P 8 animals were killed at each time point respectively and in control group the 8 animals were killed at 360 min after ip NS injection. The lungs were immediately removed. Blood and lung NO and MDA levels and RBC SOD content were measured.Results The serum and lung NO concentration measured at all 4 time points were significantly lower in group Ⅲ than those in group n (P

Objective To establish a rabbit auricular hematoma model,to observe the process of production and absorption,and to study the location of hematoma and method of its removal Methods Ten health New Zealand rabbits were divided randomly into control group and experimental group.A weight was dropped onto particular locality of auricles 3-6 times until a big hematoma appeared.The pathological processes of hematoma were observed,and the hematoma was formed 1 hour and the hematoma was almost absorbed after 4 days.The drainage experiment was conducted to observe the effect of needle aspiration or incision and drainage on the hematoma.Results All experimen tal auricles formed hematoma.The histopathological study showed that hematoma located between skin and cartilage,did not involve the cartilage.After 4 days,new-formed capillaries and fibroblasts were found,and then hematoma mostly absorbed; fibrous hyperplasia was been found.By cutting the hematoma,the blood clot could be thoroughly removed.Conclusions The auricular hematoma model can be established easily by striking with a heavy weight.Hematoma locates in subcutaneous connective tissue.A large hematoma should be early removed for prevention of auricular deformity.

Objective:To explore the mediation effect of personality between negative life events and risky mentation of university students.Methods:A cross sectional investigation was conducted among 8 379 freshmen with the adolescent self-rating life events check list (ASLEC), the prodromal questionnaire(PQ-16) and the Eysenck personality questionnaire (EPQ). The data were analyzed by SPSS 23.0 and AMOS 24.0.Results:The total score of negative life events scale((31.16±0.58) vs (15.19±0.15)), the scores of neuroticism((58.20±0.36) vs (41.59±0.13)) and psychoticism((53.07±0.29) vs (47.71±0.08)) in the risk psychological state group were significantly higher ( t=26.611, 42.270, 17.286, all P<0.01), and the score of introversion-extroversion factor was significantly lower((49.83±0.42) vs (55.88±0.13), t=-13.634, P<0.01) than those in the risk-free psychological state group. There was a positive correlation between the scores of risk psychological state and negative life events( r=0.290, 0.334, both P<0.01), and the scores of risk psychological state and negative life events were positively correlated with the scores of personality neuroticism and psychoticism ( r=0.139-0.469, all P<0.01) in both risk psychological state and risk-free psychological state group.The risk psychological state score of college students was negatively correlated with the inside and outside personality score( r=-0.070, P<0.01), and the score of negative life events was not correlated with introversion-extroversion personality score in the risk psychological state group, while the score of risk psychological state, negative life events and introversion-extroversion personality score were negatively correlated in the risk-free psychological state group ( r=-0.177, -0.080, P<0.01). The personality of college students played a complete mediating role between negative life events and risk psychological state in the risk psychological state group, while the personality of college students in the risk-free psychological state group played a partial mediating role between negative life events and risk psychological state, accounted for 71.43% of the total effect. Conclusion:Negative life events not only directly lead to the risky mentation of college students, but also affect the risky mentation of college students by the mediation effect of introverted and extroverted tendency and unstable emotion.

Objective To investigate the role of LncRNA ROR in Ad36-induced browning of human adipose-derived stem cells(hADSC). Methods After hADSC was induced by cocktail and Ad36 for 2,4,6,and 8 days,Oil red O staining was performed for observing the adipogenic status. The mRNA expressions of LncRNA ROR, uncoupling protein 1(UCP1),and PRDM16 were detected by real-time PCR and the protein expressions of UCP1 and PRDM16 were detected by Western-blot. After LncRNA ROR was knocked down by siRNA, UCP1 and PRDM16 mRNA and protein expression levels in the process of Ad36-induced adipocyte differentiation were detected by real-time PCR and Western-blot. Results Oil red O staining showed that fat droplets in the cocktail-induced group were larger than those in the Ad36-induced group. Compared with the cocktail group,the mRNA expressions of LncRNA ROR, UCP1 and PRDM16, and the protein expressions of UCP1 and PRDM16 in Ad36 group were significantly increased(P<0.05). The mRNA and protein expressions of UCP1 and PRDM16 in LncRNA ROR knockdown group were significantly lower than those in control group(P<0.05). Conclusion In the process of Ad36-induced hADSC differentiation,the up-regulation of LncRNA ROR may stimulate UCP1 and PRDM16 expression,and thus promote the browning of hADSC.

Objective To investigate the expressions of RNA-binding protein human antigen R(HuR), fatty acid binding protein type 4(FABP4),fatty acid synthetase(FASN),and lipoprotein lipase(LPL)during the differentiation of human adipocytes, and to explore their possible roles. Methods Human adipose-derived mesenchymal stem cells were induced by adipogenic differentiation,and the adipogenesis of cells was observed by oil red O staining. The expressions of HuR,FABP4,FASN,and LPL mRNA and protein were detected by real-time PCR and Western blotting. After HuR was silenced by siRNA, the change of adipogenesis for human adipose-derived mesenchymal stem cells was observed and the expressions of adipogenic genes were detected. Results The expressions of HuR,FABP4,FASN,and LPL mRNA and protein were significantly increased after human adipose-derived mesenchymal stem cells were induced to differentiate into adipocytes(all P<0.01). After HuR expression was down-regulated by siRNA,the adipogenic level of human adipose-derived mesenchymal stem cells was reduced,with decreased protein levels of FABP4,FASN,and LPL(all P<0.05),which were without changes for their mRNA levels. Conclusion HuR promotes the differentiation of human adipocytes mainly via regulating the changes of FABP4,FASN,and LPL protein levels.

Alzheimer′s disease (AD) is an incurable disease in the field of major chronic diseases. Subjective cognitive decline (SCD) is a clinical risk factor for AD. The standardized screening and intervention in individuals with SCD are of great importance in early prevention and treatment of AD. According to the clinical criteria proposed by The characterisation of subjective cognitive decline, which was published online in Lancet Neurology, the article summarized the definition of SCD, the latest perspective of clinical standards in SCD, and the results of AD preclinical SCD research. The purpose of this work was to provide concrete guidance and recommendations for making clinical decisions in diagnosis and scientific research on SCD.

Objective:To investigate the possible role of long non-coding RNA (LncRNA) 00602 in promoting browning in adipocytes induced by adenovirus type 36 (Ad36).Methods:According to Ad36 infection, adipose tissue samples of obese patients were divided into Ad36-negative group and Ad36-infected group. Realtime fluorescent quantitative PCR (qRT-PCR) was used to detect the changes in the expression of LncRNA00602 mRNA in omental adipose tissue of the two groups, and analyze the differences between the two groups. The correlation between waist-to-hip ratio, systolic blood pressure, diastolic blood pressure, fasting blood glucose, triacylglyceride and other indicators of the patients in the group with LncRNA00602 mRNA expression were analyzed. HE staining was used to detect the size of adipocytes in the omental adipose tissue of the Ad36 negative group and the Ad36 infection group. qRT-PCR and Western blotting were used to detect the mRNA and protein expression levels of uncoupling protein 1 (UCP1) and PR domain containing 16 (PRDM16) in omental adipose tissue of two groups of patients. Human adipose-derived stem cells (hADSC) were isolated and cultured, using Ad36 to induce differentiation, and divided into control group and LncRNA00602 knockdown group. On 0, 2, and 4 days after LncRNA00602 knockdown, fluoroboron dipyrrole (BODIPY) and mitochondrial red fluorescence (Mito-Tracker Red) were used to stain intracellular lipid droplets and mitochondria. At the same time, qRT-PCR and Western blotting were used to detect changes in the expression of UCP1 and PRDM16.Results:The expression of LncRNA00602 gene in the Ad36 infection group was higher than that in the Ad36 negative group (all P<0.05). The expression of LncRNA00602 in the Ad36 negative group was not significantly different from the above clinical indicators, while the expression of LncRNA00602 was negatively correlated with serum fasting blood glucose and triacylglyceride ( r=-0.522, -0.486, P<0.05) in the Ad36 infection group; HE staining showed that the average adipocyte area of the Ad36 infection group was smaller than that of the Ad36 negative group. At the same time, UCP1 and PRDM16 gene expression were higher than the negative group (all P<0.05). At the cellular level, on the 2nd and 4th days after knockdown of LncRNA00602, the lipid droplet area of adipocytes in the LncRNA00602 knockdown group was larger than that of the control group, the number of mitochondria decreased compared with the control group, and difference was statistically significant ( P<0.05 or P<0.01); Compared with the control group, there was significantly lower expression of the browning marker genes UCP1, PRDM16, and protein in the adipocytes in the LncRNA00602 knockdown group (all P<0.05). Conclusion:In Ad36-induced adipocyte differentiation, LncRNA00602 may positively regulate the expression of UCP1, PRDM16 and lipid droplet metabolism, and promote the browning of adipocytes.

Objective : To investigate the influence and molecular mechanism of hypoxia-inducing factor-1 α( HIF- 1 α) gene silencing combined with methyl selenenic acid (MSA) on cervical cancer cell proliferation，apoptosis and cell migration． Methods : HeLa cells were transfected with HIF-1 interference RNA and negative control RNA．Af- ter transfection for 48 h，cells were stimulated with MSA for 24 h，and cell proliferation was determined by CCK-8 assay and colony formation．Apoptosis was determined by flow cytometry combined with Annexin V-FITC / PI．The expression levels of HIF-1α , Bcl-2 ，and E-cadherin were detected by Western blot assay． Cell migration ability was determined by Transwell assay. RNA-seq analysis was used to investigate the differentially expressed genes and differential signaling pathways. Results : Compared with the control group，interfering with HIF-1α combined with MSA significantly inhibited cell proliferation (P ＜0．01) ．Flow cytometry results showed that the combined drug group significantly induced apoptosis．Transwell results showed that interfering with HIF-1α combined with MSA inhibited HeLa cell migration．Compared with the control group，interfering with HIF-1α combined with MSA down- regulated the expression of Bcl-2 and up-regulated the expression of E-cadherin. RNA-sequencing combined with signal pathway enrichment results showed that the expression of apoptotic signal pathway and downstream genes was inhibited． Conclusion HIF-1α gene silencing combined with MSA can synergically inhibit the proliferation and induce apoptosis of cervical cancer cells，and its regulatory mechanism may be related to the expression of Bcl-2 family proteins and the inhibition of p53 signaling pathway.

Objective To compare and analyze the differences between customized models and commercial universal models in the segmentation of organs-at-risk in cervical cancer,and to investigate the feasibility of customized models.Methods A retrospective analysis was conducted on 270 cervical cancer patients.Senior clinicians manually delineated organs-at-risk,including the bladder,rectum,small intestine,pelvic bone marrow,femoral heads,and kidneys.The cases were randomly selected to develop customized models,with 202 cases allocated to the training set,38 cases to the test set,and 30 cases to the validation set.The universal and customized models were used for segmentation on the test set,and the automatic segmentation results obtained by the two models were compared with manual segmentation results to assess the performance of the customized model.Results Both customized model and universal model had comparable DSC values to manual segmentation,demonstrating satisfactory delineation outcomes(DSC values ranging from 0.7 to 0.9).However,in terms of deviation of centroid and 95％Hausdorff distance,the customized model surpassed the universal model.Conclusion Compared with the universal model,the customized model offers superior accuracy in delineating the structures of organs-at-risk in cervical cancer.As the customized model is optimized based on specific datasets,it provides precise support for clinical decision-making and holds promising applications in the treatment of cervical cancer.

Objective: To investigate the role of adenovirus type 36 (Ad36) in the browning of 3T3-L1 cells. Methods: BODIPY staining was performed on the 0, 2nd, 4th, 6th and 8th days of the cocktail induction (control) group and the cocktail plus Ad36 induction (experimental) group to observe the adipogenesis of 3T3-L1 cells.The mRNA and protein expressions of uncoupling protein-1(Ucp1), ATP synthase, H+ transporting, mitochondrial F1 complex, O subunit (Atp5o), cytochrome c oxidase subunit 5B(Cox5b), and perilipin were detected by real-time PCR and Western-blot. Results: The results of BODIPY staining showed that the lipid droplets in the control group gradually became larger with the differentiation of the cells, while the lipid droplets in the experimental group firstly became larger, and then appeared smaller after Ad36 was added on the fourth day. Compared with the control group, the mRNA and protein expression levels of Ucp1, Atp5o, and Cox5b in the experimental group were significantly increased while the expression level of perilipin was significantly decreased (all P<0.05). Conclusion During the differentiation of 3T3-L1 cells, Ad36 promotes its browning via increasing the expressions of Ucp1, Atp5o, and Cox5b.