Objective To prepare 3D printed tracheal graft and investigate its cellular biocompatibility and biomechanical properties.Methods Bone marrow was isolated from tibial plateau of young New Zealand white rabbit,and bone mesenchymal stem cells (BMSCs) were obtained by whole bone marrow culture method and adherent purification method.Biomechanical test was performed for 3D printed trachea graft.After co-cultured of 3D printed trachea graft and BMSCs,cell morphology was observed and the proliferation index of the cells on 3D printed trachea graft was quantified using sulforhodamine B (SRB) assay.Results 3D printed trachea graft showed excellent biomechanical properties.Cell morphology was normal and cells grew well after co-culture with 3D printed trachea graft.The SRB assay indicated good proliferation of BMSCs on 3D printed trachea graft.Conclusions 3D printed trachea graft shows favorable cellular biocompatibility and biomechanical properties,and therefore can be used as a scaffold material for tissue-engineered trachea.

Tissue engineering can regenerate damaged tissues and restore the biological functions by cell or tissue reconstruction,and is becoming a promising method for trachea replacement.Seed cells,cell growth factors and tracheal scaffolds are the three major elements of tissue engineering trachea,as a result researchers have paid a lot of attention to find ideal seed cells.Mesenchymal stem cells (MSCs) are a kind of stem cells with high self-renewal ability and muhi-directional differentiation potential.MSCs are widely distributed in bone marrow,umbilical cord,adipose tissue,myocardial tissue,brain,muscle and skin,and can differentiate into a variety of cells,including osteocytes,chondrocytes,adipocytes and neurocytes.MSCs have the characteristics of high proliferation ability,wide differentiation range and immunomodulatory function,which can be used to repair damaged tissue.These advantages make the MSCs an ideal candidate of seed cells for tissue engineering trachea.This review mainly summarized the application of MSCs in tissue engineering trachea.

AIM:To investigate the role of anti-miR-21 oligonucleotide ( AMO) in the anti-leukemic activity of decitabine (DCA) in vitro.METHODS:AMO and scramble oligonucleotide (SCR) were constructed and transfected into HL-60 cells.The miR-21 expression was analyzed by real-time PCR to identify the transfection efficiency .The cells were treated with DCA at gradient concentrations (0.5, 2.0 and 4.0 μmol/L) for 48 h.The mRNA expression of human period circadian protein 3 (hPer3) was detected by real-time PCR.The early apoptotic rates were determined by flow cy-tometry with Annexin V/PI staining.Mean fluorescence intensities ( MFI) of CD117 and CD11b were also measured by flow cytometry.RESULTS:The miR-21 relative expression level in AMO group was significantly lower than that in blank group and SCR group (P<0.01).IC50 of DCA in AMO group was significantly lower than that in blank group and SCR group (P<0.01).With the same concentration of DCA, the early apoptotic rate, the mRNA expression of hPer3 and the MFI of CD11b in AMO group were significantly higher than those in blank group and SCR group (P<0.01).The MFI of CD117 in AMO group were significantly lower than those in blank group and SCR group ( P<0.01 ) .CONCLUSION:Activation of hPer3 expression plays an important role in enhanced anti-leukemic activity of decitabine by AMO in vitro.

To investigate the osteogenesis characteristics of cultured rat mesenchymal stem cells (MSCs) under bone induction condition.

OBJECTIVETo investigate the health status of the thyroid and related influencing factors in the seamen in Zhoushan, China.

METHODSA total of 136 coastal seamen (coastal group), 104 deep-sea seamen (deep-sea group), and 272 base staff (base group) who underwent physical examinations in 2014 were selected. Questionnaire survey and ultrasound were performed, and levels of thyroid hormone and urinary iodine were measured.

RESULTSCompared with the coastal group and the base group, the deep-sea group had a significantly higher rate of abnormal ultrasound findings (49.04% vs 30.88%/28.67%, P<0.05), as well as a significantly higher rate of abnormal serum free thyroxine (FT4) (25.00% vs 9.56%/6.25%, P<0.05). The logistic regression analysis showed that in the coastal group, the risk factors for thyroid abnormality on ultrasound were obesity shown by body mass index (BMI) (OR=2.55, 95% CI=1.13~4.13) and annual working time>6 months (OR=4.25, 95% CI=2.02~8.26) (both P<0.05); in the deep-sea group, the risk factors for thyroid abnormality on ultrasound were obesity shown by BMI (OR=3.45, 95% CI=1.28~7.02) and annual working time>6 months (OR=5.33, 95% CI=3.18~9.23) (both P<0.05).

CONCLUSIONThe thyroid abnormality in deep-sea seamen is caused by various reasons and is correlated with annual working time, working environment and area, and iodine nutritional status.

Body Mass Index ; China ; Health Status ; Humans ; Iodine ; urine ; Male ; Naval Medicine ; Occupations ; Risk Factors ; Surveys and Questionnaires ; Thyroid Function Tests ; Thyroid Gland ; diagnostic imaging ; pathology ; Thyroxine ; blood ; Ultrasonography

Objective To find out whether conversation analysis helps to differentiate psychogenic nonepileptic seizure (PNES) from epileptic seizure in Chinese patients.Methods Twelve unselected patients from Peking Union Medical College Hospital during 2014 to 2016 with diagnostic uncertainty were included.Interactions following standard protocol were carried out.A linguist blinded to all medical data and a neurologist studied videos and transcripts of the interactions.Using a diagnostic scoring aid which includes 17 conversation features summarized from previous researches, they attempted to predict the medical diagnosis of those patients independently.Results Accurate diagnosis was predicted in 10/12 patients by both raters.Average scores of patients with epileptic seizures were 8.00 (linguist) and 6.75 (neurologist), while average scores of paitents with PNES were-5.75 (linguist) and-7.88 (neurologist).Both raters agreed on most individual items (81.86%, 167/204).To demonstrate different features between these two groups, a case comparison was made between one patient with frontal lobe epilepsy and one patient with PNES.Conclusion In Chinese patients, conversation analysis can help differentiate between epileptic seizure and PNES.

AIM:To investigate the inhibitory effect of apolipoprotein A-I mimetic peptide D-4F on the scaven-ger receptor A1 ( SR-A1 ) in macrophage-derived foam cells induced by oxidized low-density lipoprotein ( ox-LDL ) . METHODS:RAW264.7 cells were pretreated with different concentrations (12.5, 25 and 50 mg/L) of D-4F or 50 mg/L inactive control peptide scrambled D-4F (sD-4F) for 1 h or endoplasmic reticulum stress (ERS) inhibitor 4-phenylbutyr-ic acid (5 mmol/L) for 30 min, followed by the treatment with 100 mg/L ox-LDL for 12 h.In addition, the cells were pre-treated with 50 mg/L D-4F or sD-4F for 1 h, and then stimulated with 2 mg/L tunicamycin (TM;an ERS inducer), for 4 h.The viability of the cells was measured by MTT assay, and the content of intracellular total cholesterol ( TC) was meas-ured by a tissue/cell TC assay.The protein and mRNA levels of SR-A1 and glucose-regulated protein 78 (GRP78) were analyzed by Western blotting and quantitative real-time PCR, respectively.The fluorescence intensity of DiI-ox-LDL in the cells was detected by a multifunctional microplate reader.RESULTS:D-4F significantly reduced ox-LDL-induced macro-phage injury and intracellular cholesterol accumulation, and attenuated the ox-LDL-induced expression of SRA1 and GRP78 in a dose-dependent manner.Additionally, D-4F significantly inhibited the TM-induced protein expression of SR-A1 and GRP78, and attenuated the uptake of ox-LDL by macrophages.CONCLUSION: D-4F reduces ox-LDL-induced macro-phage cholesterol accumulation and injury by inhibiting SR-A1 expression.The mechanism may be related to the inhibition of ERS signaling pathway mediated by GRP78.

Objective To construct luciferase reporter vector containing full-length high-mobility group box 1 ( HMGB1, GenBank NM-010439) promoter for the screening of medicine. Methods The full-length HMGB1 promoter was amplified by polymerase chain reaction ( PCR) , and then was inserted into GV238 vector to construct plasmid GV238-HMGB1-P-Luc. GV238-HMGB1-P-Luc combined with internal reference plasmid pRL was co-transfected into Hela cells ( GV238-HMGB1-P-Luc group, which served as positive control group) . Plasmid pGL3-basic combined with pRL was co-transfected into Hela cells (pGL3-basic group, which served as negative control group) . Additionally, lipopolysaccharides ( LPS, 0.2 μg/mL) was used as the activator for the positive control group (LPS group), and then sodium butyrate (SB, 10 mmol/L) was used as the inhibitor for LPS group ( SB group) . At the end of experiment hour 24, luciferase activity was detected. Results The results of digestion, amplification, sequencing and identification showed that the full length of HMGB1 promoter was 2 140 bp, and the DNA sequence was correct, without mutation. Luciferase activity in GV238-HMGB1-P-Luc group was increased as compared with that of the pGL3-basic group ( P<0.05) . Luciferase activity in the LPS group was increased ( P<0.01, compared with that of GV238-HMGB1-P-Luc group) , and then was decreased after the administration of SB ( P<0.01, compared with that of the LPS group) . Conclusion A model of luciferase reporter vector containing HMGB1 promoter has been successfully constructed. Its activity can be increased by LPS, and then is in hibited by SB. The model can be used for further screening of medicine with the activities of regulating HMGB1 promoter.

Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with chronic inflammation in the vascular wall while its specific pathogenesis is not fully understood. Recently, a growing number of studies have indicated that pyroptosis, which is a pro-inflammatory kind of programmed cell death might play a vital role in AAA. In this review, we first summarize the role of pyroptosis in AAA progression by not only providing a literature review on the expression changes of NLRP3 inflammasome components and effector mediators in clinical and experimental AAAs, but also discussing the effects of genetic defects or pharmacological inhibition of NLRP3 inflammasome components on experimental AAAs. Next, we introduce the mechanism of canonical and non-canonical pathway of pyroptosis and its activation and execution process. Finally, we discuss several pyroptosis-related drug targets for treating AAA by inhibiting the assembly of NLRP3 inflammasome and its effector mediators. In conclusion, we believe that pyroptosis might be a new treatment target of AAA.

Objective:To investigate the effect of IKKε on autophagy during abdominal aortic aneurysm formation in mice.Methods:We stimulated ApoE -/- mice and ApoE -/-IKKε -/- mice with AngⅡ and saline for 28 days. Metaboilic levels and aortic diameter of ApoE -/- mice and ApoE -/-IKKε -/- mice were measured. The arterial fibrosis of mice was detected by Masson staining and HE staining, mitochondrial reactive oxides were detected by fluorescence assay, the expression levels of autophagy factors LC3B and Beclin-1 were detected by immunohistochemistry, and the protein level of LC3B was detected by Western blot. Results:There was no significant difference in metaboilic levels between ApoE -/- mice and ApoE -/- IKKε -/- mice. However, the aortic diameterf ApoE -/-IKKε -/- mice was significantly less than that of ApoE -/- mice. The fibrosis level of ApoE -/-IKKε -/- mice was significantly lower than that of ApoE -/- mice. Furthermore, ROS in ApoE -/-IKKε -/- mice was lower than that in ApoE -/- mice. In addition, immunohistochemical and western blot showed that the expression levels of LC3B and Beclin-1 in ApoE -/-IKKε -/- mice were significantly lower than in ApoE -/- mice. Conclusion:IKKε -/- deficiency can significantly inhibit autophagy, thus reducing the development of abdominal aortic aneurysm in mice.