Prediction of new vertebral compression fracture within 3 years after percutaneous vertebroplasty for osteoporotic vertebral compression fracture: Establishment and validation of a nomogram prediction model.

New vertebral compression fractures (NVCF) are common in patients with osteoporotic vertebral compression fractures (OVCF) who have undergone percutaneous vertebroplasty (PVP). We sought to develop a nomogram prediction model for better identification and prevention of NVCF within 3 years after PVP in patients with OVCF. The demographic, clinical, and imaging data of patients who underwent PVP for OVCF between January 2010 and December 2019 were reviewed. Multivariate logistic regression analysis was used to screen for risk factors for NVCF within 3 years after PVP. A nomogram prediction model was then developed and validated to visually predict NVCF. The samples in the model were randomly divided into training and validation sets at a ratio of 7:3. Twenty-seven percent of patients experienced NVCF in other segments within 3 years after PVP. Older age, lower bone mineral density (BMD), smoking, lack of anti-osteoporosis therapy, and postoperative trauma were risk factors for NVCF. The area under the receiver operating characteristic curve suggested good discrimination of this model: training set (0.781, 95% confidence interval: 0.731-0.831) and validation set (0.786, 95% confidence interval: 0.708-0.863). The calibration curve suggested good prediction accuracy between the actual and predicted probabilities in the training and validation sets. The DCA results suggested that, when the probability thresholds were 0.0452-08394 and 0.0336-0.7262 in the training and validation set, respectively, patients can benefit from using this model to predict NVCF within 3 years after PVP. In conclusion, this nomogram prediction model that included five risk factors (older age, lower BMD, smoking, postoperative minor trauma, and lack of anti-osteoporosis treatment can effectively predict NVCF within 3 years after PVP. Postoperative smoking cessation, standard anti-osteoporosis treatment, and reduction in incidental minor trauma are necessary and effective means of reducing the incidence of NVCF.

Long-term outcome of percutaneous vertebroplasty versus conservative treatment for osteoporotic vertebral compression fractures: a retrospective cohort study with three-year follow-up.

Background: Osteoporotic vertebral compression fractures (OVCF) appear to be more common as the population ages. Previous studies have found that percutaneous vertebroplasty (PVP) can achieve better short-term clinical outcomes than conservative treatment (CT) for OVCF. However, the long-term outcomes of PVP compared with CT for OVCF has been rare explored. This study was designed to explore the clinical outcomes of PVP or CT within 3 years after OVCF. Methods: This study reviewed the clinical outcomes of patients who underwent PVP or CT for OVCF in a single center from January 2015 to December 2019. The back pain visual analogue scale (VAS), Oswestry disability index (ODI) and satisfaction rate were compared between the two groups at baseline, 1 week, 1 month, 3 months, 6 months, 12 months, 24 months and 36 months after treatment. Outcomes: The baseline data including gender, age, bone mineral density, body mass index, back pain VAS, and ODI were not significantly different between the two groups. The back pain VAS and ODI of CT patients were significantly higher than those of PVP group at 1 week, 1 month, 3 months, 6 months and 12 months after treatment. The satisfaction rate in the PVP group were significantly higher than those in the CT group at 1 week, 1 month, 3 months and 6 months after treatment. Subsequently, the back pain VAS and ODI showed no significant difference between the two groups at 24 and 36 months. In addition, there was no significant difference in treatment satisfaction between the two groups at 36 months. There was no significant difference in the rate of new vertebral compression fractures between the two groups within 36 months after treatment. Conclusion: The clinical outcomes within 12 months after PVP and patient satisfaction rate within 6 months after PVP were significantly higher than CT. However, during 12 months to 36 months, this advantage generated by PVP was gradually diluted over time. Compared with CT, the long-term effect of PVP on OVCF should not be overestimated.

Warming in combination with increased precipitation mediate the sexual and clonal reproduction in the desert steppe dominant species Stipa breviflora.

BACKGROUND: Clonal plants can successfully adapt to various ecosystems. A trade-off between sexual and clonal reproduction is generally assumed in clonal plants, which may be influenced both by the characteristics of the plant itself and environmental conditions. Currently, it is unclear how climate change, and specifically warming and increased precipitation, might affect sexual and clonal reproduction in clonal plants. Therefore, this study aimed to investigate both the sexual and clonal reproduction responses of Stipa breviflora to warming and increased precipitation. A controlled experiment was conducted by inducing increases in precipitation (ambient condition, 25% and 50% increases) and warming (ambient temperature, 1.5 °C and 3.0 °C increases). RESULTS: Warming significantly influenced both the ratio of reproductive ramet shoot biomass to total shoot biomass, and the ratio of reproductive ramet number to total ramet number. Additionally, the ratio of reproductive ramet shoot biomass to total shoot biomass was also significantly affected by increased precipitation. Increased precipitation benefited sexual reproduction, while effects of warming on reproductive and/or vegetative ramets varied from negative to positive depending on precipitation conditions. There was no relationship between the number or shoot biomass of reproductive ramets and vegetative ramets. Reproductive ramets displayed greater sensitivity to climate change than vegetative ramets. CONCLUSIONS: The findings of our study suggest that there was no trade-off between sexual and clonal reproduction in S. breviflora. The combined impact of warming and increased precipitation promoted sexual reproduction but did not inhibit clonal reproduction. Clonal plants with the capacity for both sexual and clonal reproduction, may cope with climate change well via clonal reproduction, ensuring their survival.

The impact of organic fertilizer replacement on greenhouse gas emissions and its influencing factors.

Although organic fertilizers played an important role in enhancing crop yield and soil quality, the effects of organic fertilizers replacing chemical fertilizers on greenhouse gas (GHG) emissions remained inconsistent, and further impeding the widespread adoption of organic fertilizers. Therefore, a global meta-analysis used 568 comparisons from 137 publications was conducted to evaluate the responses of GHG emissions to organic fertilizers replacing chemical fertilizers. The results indicated that organic fertilizers replacing chemical fertilizers significantly decreased N2O emissions, but increasing global warming potential (GWP) by enhancing CH4 and CO2 emissions. When replacing chemical fertilizers with organic fertilizers, a variety of factors such as climate conditions, soil conditions, crop types and agricultural practices influenced the GHG emissions and GWP. Among these factors, fertilizer organic C and available N level were the main factors affecting GHG and GWP. However, considering the feasibility and ease of optimizing these factors, fertilizer organic C, C/N and N substitution rate showed a more favorable choice for GWP reduction, and their interactions significantly affecting GWP. Moreover, considering the distinct GHG emissions patterns in dryland and paddy field, the analysis of optimizing GWP based on fertilizer organic C, C/N and N substitution rate was separately conducted. According to the simulation optimization, the optimal combination of fertilizer organic C (137.2-228.8 g·kg-1), C/N (6.9-52.0) and N substitution rate (20.0-22.5 %) effectively suppressed the extent of increase in GWP in paddy field compared with chemical fertilizers. In dryland, optimizing fertilizer organic C (100-278 g·kg-1), C/N (70.7-76.6) and N substitution rate (10.2-16.0 %) led to a reduction in GWP compared with chemical fertilizers, indicating that dryland are more suitable for promoting organic fertilizer application. In conclusion, this meta-analysis study quantitatively assessed the GHG emissions when organic fertilizers replacing chemical fertilizers, and also provided a scientific basis for the mitigation of GHG emissions by organic fertilizers management.

Development of a novel and fast XRF instrument for large area heavy metal detection integrated with UAV.

The disadvantages of the current chemical and instrumental analysis methods for soil heavy metal pollution are that they have a high detection cost, long cycle times, and may cause secondary pollution. The aims of this study were to improve the rapid detection of soil heavy metal pollution over large areas. This study combined aircraft technology, embedded development, computer software, electronic information, and other technical methods to create a novel solution to the problem, i.e., an integrated unmanned aerial vehicle (UAV) based soil heavy metal pollution rapid detection system (UAV-SHMPRDS) was built. The key technologies required for a rapid detection system were developed, including the development of a hardware system based on a UAV and an X-ray fluorescence spectrum (XRF) analyzer, the design and implementation of a control system software system, and the implementation of a data inversion processing algorithm. Finally, a prototype UAV-SHMPRDS was constructed. Testing showed that the system improved regionalized soil heavy metal pollution detection efficiency. This study provides new solutions for the current problems encountered in the actual rapid detection of soil heavy metal pollution.

Circ_0114427 promotes LPS-induced septic acute kidney injury by modulating miR-495-3p/TRAF6 through the NF-κB pathway.

BACKGROUNDS: Septic acute kidney injury (AKI) is a severe illness in clinics. Enriching researches investigated the regulatory network of AKI during the past decades, evidences showed that circular RNAs (circRNAs) were involved in the molecular mechanism of human AKI. However, the special responses remain largely elusive. Thus, the study aims to investigate the function of circ_0114427 in the progression of AKI. METHODS: The levels of circ_0114427, miR-495-3p and Tumour Necrosis Factor Receptor-Associated Factor 6 (TRAF6) were both assessed by quantitative real-time polymerase chain reaction (qRT-PCR). In addition, lipopolysaccharide (LPS) was applied to establish AKI cell model, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was carried out to determine the viability of LPS-induced HK-2 cells. The expression of TRAF6, B-cell lymphoma-2 (Bcl-2), Bcl2-associated X (Bax), cleave-caspase 3, caspase 3, total IκBα (t-IκBα), phospho-IκBα (p-IκBα), total p65 (t-p65) and phospho-p65 (p-p65) were all detected via western blot. The levels of IL-1ß and TNF-α were identified by western blot and ELISA. What's more, cell apoptosis was measured by flow cytometry. Lastly, dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assays were employed to verify the relationships between miR-495-3p and circ_0114427 or TRAF6 in vitro. RESULTS: The level of miR-495-3p was remarkably restrained while circ_0114427 and TRAF6 levels were specially reinforced in AKI patient serum samples and LPS-induced HK-2 cells. Moreover, IL-1ß and TNF-α were highly expressed in LPS-induced AKI cells. Functionally, circ_0114427 was a sponge of miR-495-3p, and circ_0114427 silence-mediated effects in LPS-induced HK-2 cells were partly ameliorated by the addition of miR-495-3p inhibitor. Moreover, TRAF6 was a target gene of miR-495-3p, and the inhibiting effect of miR-495-3p on cell apoptosis and inflammatory response was mitigated by TRAF6 overexpression. Mechanistically, the circ_0114427/miR-495-3p/TRAF6 axis modulated cell apoptosis and inflammatory response via NF-κB/p65 signalling pathway in AKI. CONCLUSION: Circ_0114427 regulated cell apoptosis and inflammatory response through miR-495-3p/TRAF6 axis via NF-κB/p65 signalling pathway, providing a novel mechanism in clinical treatment of AKI patients.HighlightsCirc_0114427 is upregulated in serum specimens from septic AKI patients and LPS-induced HK-2 cells.LPS treatment suppresses cell viability and promotes apoptosis and inflammation in HK-2 cells.Circ_0114427 knockdown ameliorates the effects of LPS on cell viability, apoptosis and inflammation in HK-2 cells.Circ_0114427 regulates LPS-induced HK-2 cell injury by regulating miR-495-3p/TRAF6/NF-κB/p65 axis.

Type 2 Diabetes Mellitus Easily Develops into Alzheimer's Disease via Hyperglycemia and Insulin Resistance.

With the acceleration of population aging, the incidence of type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) is progressively increasing due to the age-relatedness of these two diseases. The association between T2DM and AD-like dementia is receiving much attention, and T2DM is reported to be a significant risk factor for AD. The aims of this review were to reveal the brain changes caused by T2DM as well as to explore the roles of hyperglycemia and insulin resistance in the development of AD.

Generation of a laminopathies-specific iPSC line EHTJUi005-A-3 with homozygous knockout of the LMNA gene by CRISPR/Cas9 technology.

LAMIN A/C, encoded by the LMNA gene, supports the normal structure of the cell nucleus and regulates the connection between the nucleus and the cytoskeleton as a component of the nucleus envelope. The loss of expression and function of the LMNA gene would lead to the occurrence of congenital muscular dystrophy and Emery-Dreifuss muscular dystrophy which are collectively named as laminopathies. Here, we report a human induced pluripotent stem cell (iPSC) line (EHTJUi005-A-3) generated from a wild iPSC (EHTJUi005-A) with homozygous knockout of the gene LMNA through CRISPR/Cas9. This iPSC line provides a useful research model for studying laminopathies disease.

CRISPR/Cas9 mediated generation of a iPSC line EHTJUi005-A-1 with homozygous knockout of the SUV39H1 gene.

SUV39H1 is a histone methyltransferase involve numerous biological processes, including of aging, embryo development, tumor growth and mitosis via catalysis of dimethylation and trimethylation of lysine 9 of histone H3. Here we report a human induced pluripotent stem cell line (EHTJUi005-A-1) which is generated from a wildtype human iPSC previously established in our laboratory, and this iPSC has a homozygous knockout of 8 bp in Exon 2 of SUV39H1. This iPSC model provides a valuable resource to study epigenetic regulation in extensive biological processes as mentioned above.

An induced pluripotent stem cell line (EHTJUi003-A) generated from a neonate with c.1377delC mutation in the gene MYBPC3 causing hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant heart disease. An induced pluripotent stem cell line (EHTJUi003-A) was generated from umbilical cord blood mononuclear cells (UCBMCs) of a female neonate with heterozygous mutation of p.L460Wfs (c.1377delC) in the MYBPC3 gene. This iPSC model offers a very valuable resource to study the pathological mechanism of HCM in vitro.

An induced pluripotent stem cell line (EHTJUi004-A) generated from a neonate with c.4683_4684delCT:p.Leu1563fs mutation in the gene DSP causing Familial Arrhythmogenic Right Ventricular Dysplasia (ARVD).

Familial Arrhythmogenic Right Ventricular Dysplasia (ARVD) is a primary cardiomyopathy characterized by the abnormality of the right ventricular muscle. ARVD may be life-threatening due to the induction of paroxysmal refractory ventricular tachycardia or supraventricular arrhythmia. A human induced pluripotent stem cell line (EHTJUi004-A) was generated from human umbilical cord blood mononuclear cells (UCBMCs) of a female neonate with heterozygous mutation of p.Leu1563fs (c.4683_4684delCT) in the DSP gene. This iPS cell line resource provides an ideal in vitro model to study the pathological mechanism of ARVD.

Repeated Restraint Stress Led to Cognitive Dysfunction by NMDA Receptor-Mediated Hippocampal CA3 Dendritic Spine Impairments in Juvenile Sprague-Dawley Rats.

Although numerous studies have indicated that chronic stress causes cognitive dysfunction with the impairment of synaptic structures and functions, the relationship between cognitive deficits induced by repeated restraint stress and the level of NMDA receptors in the subregion of the hippocampus has been relatively unknown until now. In this study, 3-week-old male Sprague-Dawley rats were exposed to repeated restraint stress for seven consecutive days, their cognitive functions were evaluated through behavioral tests, and then they were sacrificed for electrophysiological, morphological, and biochemical assays. Chronic repeated restraint stress led to cognitive and electrophysiological impairments, with a reduced density of dendritic spines. We also found that the protein level of NMDA receptors only increased in the hippocampal CA3 region. Nevertheless, repeated restraint stress-induced cognitive and synaptic dysfunction were effectively reversed by Ro25-6981, an inhibitor of the GluN2B receptor. These findings suggest that repeated restraint stress-induced synaptic and cognitive deficits are probably mediated through NMDA receptors.

Etv5 safeguards trophoblast stem cells differentiation from mouse EPSCs by regulating fibroblast growth factor receptor 2.

Previous studies have demonstrated that transcription factor Etv5 plays an important role in the segregation between epiblast and primitive endoderm at the second fate decision of early embryo. However, it remains elusive whether Etv5 functions in the segregation between inner cell mass and trophectoderm at the first cell fate decision. In this study, we firstly generated Etv5 knockout mouse embryonic stem cells (mESCs) by CRISPR/Cas9, then converted them into extended potential stem cells (EPSCs) by culturing the cells in small molecule cocktail medium LCDM (LIF, CHIR99021, (S)-(+)-dimethindene maleate, minocycline hydrochloride), and finally investigated their differentiation efficiency of trophoblast stem cells (TSCs). The results showed that Etv5 knockout significantly decreased the efficiency of TSCs (CDX2+) differentiated from EPSCs. In addition, Etv5 knockout resulted in higher incidence of the differentiated cells with tetraploid and octoploid than that from wild type. Mechanistically, Etv5 was activated by extracellular-signal-regulated kinase (ERK) signaling pathway; in turn, Etv5 had a positive feedback on the expression of fibroblast growth factor receptor 2 (FGFR2) which lies upstream of ERK. Etv5 knockout decreased the expression of FGFR2, whose binding with fibroblast growth factor 4 was essentially needed for TSCs differentiation. Collectively, the findings in this study suggest that Etv5 is required to safeguard the TSCs differentiation by regulating FGFR2 and provide new clues to understand the specification of trophectoderm in vivo.

Monomeric C-reactive protein affects cell injury and apoptosis through activation of p38 mitogen-activated protein kinase in human coronary artery endothelial cells.

C-reactive protein (CRP) is an important predictor of cardiovascular events and plays a role in vascular inflammation and vessel damage. The aim of this study was to investigate the effect of pentameric CRP (pCRP) and monomeric CRP (mCRP) on the production of atherosclerosis-re-lated factors in cultured human coronary artery endothelial cells (HCAECs). HCAECs were treated with pCRP, mCRP, p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580, or transfected with p38 MAPK siRNA. Western blotting was performed to detect the expression of vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), intercellular adhesion molecule-2 (ICAM-2) and vascular cell adhe-sion molecule-1 (VCAM-1). Proliferation, damage, and apoptosis of HCAECs were examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, lactate dehydrogenase (LDH), and flow cytometry, respectively. mCRP suppressed VEGF and COX-2 expression and enhanced ICAM-2 and VCAM-1 expression in HCAECs, in both dose-dependent and time-dependent manner. Except at 100 µg/ml concen-tration and 20-hour or 24-hour incubation, pCRP had no apparent effects. mCRP but not pCRP induced HCAEC injury and phosphorylation of p38 MAPK, and the inhibitor SB203580 reversed the effects of mCRP. mCRP promotes injury and apoptosis of HCAECs through a p38 MAPK-dependent mechanism, which provides a new therapy for the injury of HCAECs in atherosclerosis.

Molecular network of miR-1343 regulates the pluripotency of porcine pluripotent stem cells via repressing OTX2 expression.

Porcine OTX2 was found to be highly activated in porcine iPS cells (piPSCs) that were reported by different laboratories worldwide. To reveal the regulatory function of OTX2 in porcine reprogrammed cells, we screened porcine miRNA-seq databases and found two miRNAs, miR-1343 and miR-545, that could specifically bind to 3'UTR of OTX2 and suppress endogenous OTX2 expression in piPSCs. Knockdown of OTX2 by miR-1343 and miR-545 could significantly increase the expression of SOX2 and ESRRB, but did not alter the expressions of OCT4 and KLF4, and improve the pluripotency of piPSCs. The promoter-based assays showed that OTX2 potentially bound to the promoter region of SOX2 and ESRRB and suppressed their expression. On the other hand, SOX2 could interact with OTX2 promoter. Ectopic expression of SOX2 could significantly decrease OTX2 promoter activity, showing that there is a negative feedback loop between SOX2 and OTX2. Additionally, SOX2 and ESRRB significantly stimulated miR-1343 expression in piPSCs, but OTX2 down regulated the expression of miR-1343 in either direct or indirect manners. In summary, this study demonstrates that there is a regulatory network mediated by miR-1343, in which downregulation of OTX2 by miR-1343 can elevate the expression of pluripotent genes that were then sustain the pluripotency of piPSCs.

The oncogene Etv5 promotes MET in somatic reprogramming and orchestrates epiblast/primitive endoderm specification during mESCs differentiation.

Unipotent spermatogonial stem cells (SSCs) can be efficiently reprogrammed into pluripotent stem cells only by manipulating the culture condition, without introducing exogenous reprogramming factors. This phenotype raises the hypothesis that the endogenous transcription factors (TFs) in SSCs may facilitate reprogramming to acquire pluripotency. In this study, we screened a pool of SSCs TFs (Bcl6b, Lhx1, Foxo1, Plzf, Id4, Taf4b, and Etv5), and found that oncogene Etv5 could dramatically increase the efficiency of induced pluripotent stem cells (iPSCs) generation when combined with Yamanaka factors. We also demonstrated that Etv5 could promote mesenchymal-epithelial transition (MET) at the early stage of reprogramming by regulating Tet2-miR200s-Zeb1 axis. In addition, Etv5 knockdown in mouse embryonic stem cells (mESCs) could decrease the genomic 5hmC level by downregulating Tet2. Furthermore, the embryoid body assay revealed that Etv5 could positively regulate primitive endoderm specification through regulating Gata6 and negatively regulate epiblast specification by inhibiting Fgf5 expression. In summary, our findings provide insights into understanding the regulation mechanisms of Etv5 under the context of somatic reprogramming, mESCs maintenance, and differentiation.

Cardiac rehabilitation in acute myocardial infarction patients after percutaneous coronary intervention: A community-based study.

BACKGROUND: Acute myocardial infarction (AMI) is one of the leading causes of death and physical disability worldwide. However, the development of community- based cardiac rehabilitation (CR) in AMI patients is hysteretic. Here, we aimed to evaluate the safety and efficacy of CR applied in the community in AMI patients who underwent percutaneous coronary intervention (PCI). METHODS: A total of 130 ST-segment elevated myocardial infarction (STEMI) patients after PCI were randomly divided into 2 groups in the community, rehabilitation group (n = 65) and control group (n = 65). Cardiac function, a 6-minute walk distance, exercise time and steps, cardiovascular risk factors were monitored respectively and compared before and after the intervention of 2 groups. The software of EpiData 3.1 was used to input research data and SPSS16.0 was used for statistical analysis. RESULTS: After a planned rehabilitation intervention, the rehabilitation group showed better results than the control group. The rehabilitation group had a significant improvement in recurrence angina and readmission (P < .01). Left ventricular ejection fraction (LVEF) of rehabilitation group showed improvement in phase II (t = 4.963, P < .01) and phase III (t = 11.802, P < .01), and the New York Heart Association (NYHA) classification was recovered within class II. There was a significant difference compared with before (Z = 7.238, P < .01). Six minutes walking distance, aerobic exercise time, and steps all achieved rehabilitation requirements in rehabilitation group in phase II and III, there existed distinct variation between 2 phases. Rehabilitation group had a better result in cardiovascular risk factors than control group (P < .05). CONCLUSION: Community-based CR after PCI through simple but safe exercise methods can improve the AMI patient's living quality, which includes increasing cardiac ejection fraction, exercise tolerance, and physical status. It must be emphasized that the good result should be established by the foundation of close cooperation between cardiologists and general practitioners, also the importance of cooperation of patients and their families should not be ignored. The rehabilitation program we used is feasible, safe, and effective.

Fabrication of CeO2-MO x (M = Cu, Co, Ni) composite yolk-shell nanospheres with enhanced catalytic properties for CO oxidation.

CeO2-MO x (M = Cu, Co, Ni) composite yolk-shell nanospheres with uniform size were fabricated by a general wet-chemical approach. It involved a non-equilibrium heat-treatment of Ce coordination polymer colloidal spheres (Ce-CPCSs) with a proper heating rate to produce CeO2 yolk-shell nanospheres, followed by a solvothermal treatment of as-synthesized CeO2 with M(CH3COO)2 in ethanol solution. During the solvothermal process, highly dispersed MO x species were decorated on the surface of CeO2 yolk-shell nanospheres to form CeO2-MO x composites. As a CO oxidation catalyst, the CeO2-MO x composite yolk-shell nanospheres showed strikingly higher catalytic activity than naked CeO2 due to the strong synergistic interaction at the interface sites between MO x and CeO2. Cycling tests demonstrate the good cycle stability of these yolk-shell nanospheres. The initial concentration of M(CH3COO)2·xH2O in the synthesis process played a significant role in catalytic performance for CO oxidation. Impressively, complete CO conversion as reached at a relatively low temperature of 145 °C over the CeO2-CuO x -2 sample. Furthermore, the CeO2-CuO x catalyst is more active than the CeO2-CoO x and CeO2-NiO catalysts, indicating that the catalytic activity is correlates with the metal oxide. Additionally, this versatile synthesis approach can be expected to create other ceria-based composite oxide systems with various structures for a broad range of technical applications.

Common microRNA-mRNA interactions exist among distinct porcine iPSC lines independent of their metastable pluripotent states.

Previous evidences have proved that porcine-induced pluripotent stem cells (piPSCs) could be induced to distinctive metastable pluripotent states. This raises the issue of whether there is a common transcriptomic profile existing among the piPSC lines at distinctive state. In this study, we performed conjoint analysis of small RNA-seq and mRNA-seq for three piPSC lines which represent LIF dependence, FGF2 dependence and LFB2i dependence, respectively. Interestingly, we found there are 16 common microRNAs which potentially target 13 common mRNAs among the three piPSC lines. Dual-luciferase reporter assay validated that miR-370, one of the 16 common microRNAs, could directly target the 3'UTR of LIN28A. When the differentiation occurred, miR-370 could be activated in piPSCs and switched off the expression of LIN28A. Ectopic expression of miR-370 in piPSCs could reduce LIN28A expression, decrease the alkaline phosphatase activity, slow down the proliferation, and further cause the downregulation of downstream pluripotent genes (OCT4, SOX2, NANOG, SALL4 and ESRRB) and upregulation of differentiation relevant genes (SOX9, JARID2 and JMJD4). Moreover, these phenotypes caused by miR-370 could be rescued by overexpressing LIN28A. Collectively, our findings suggest that a set of common miRNA-mRNA interactions exist among the distinct piPSC lines, which orchestrate the self-renewal and differentiation of piPSCs independent of their metastable pluripotent states.

Abnormal expression of WIF1 in hepatocellular carcinoma cells and its regulating effect on invasion and metastasis factors of TIMP-3 and caveolin-1 of hepatocellular carcinoma.

OBJECTIVE: To discuss the abnormal expression of Wnt inhibitory factor (WIF1) in hepatocellular carcinoma cells and its regulating effect on the hepatocellular carcinoma invasion and metastasis factors of tissue inhibitor of matrix metalloproteinases-3 (TIMP-3) and caveolin-1. METHODS: RT-PCR and Western blot were employed to detect the expression of WIF1 in six hepatocellular carcinoma cell lines of HepG2, Hep3B, Huh7, PLC/PRF/5, SMMC-7721 and MHCC97 and the immortalized human liver cell line THLE-3. Besides, Lipofectamine 2000 was employed to transfect the eukaryotic expression vector pcDNA3.1-WIF1 and blank plasmid pcDNA3.1 into hepatocellular carcinoma cell lines. Transwell assay was used to detect the effect of WIF1 on the invasion ability of hepatocellular carcinoma cells; Western blot was used to detect the effect of WIF1 on the expression of TIMP-3 and caveolin-1 in hepatocellular carcinoma cells, it also discussed the effect on the expression of ß-catenin. RESULTS: The expression of WIF1 in hepatocellular carcinoma cell lines was lower than that in the normal liver cell lines (P < 0.01); while there was basically no expression of WIF1 in the human highly metastatic cell line MHCC-97 and moderate expression in HepG2 and SMMC-7721. Therefore, HepG2 and SMMC-7721 were chosen as the further experimental cell lines. After transfecting the eukaryotic expression vector pcDNA3.1-WIF1 and blank plasmid pcDNA3.1 into hepatocellular carcinoma cell lines, compared with the blank plasmid group, the cell viability and invasion ability in the WIF1 group were all reduced (P < 0.01), the expression of TIMP-3, caveolin-1 and mRNA were all down-regulated (P < 0.01), and the expression of ß-catenin was decreased (P < 0.01). CONCLUSIONS: Because of down-regulation or missing of expression of WIF1 in hepatocellular carcinoma cell lines, the up-regulation of WIF1 expression can significantly inhibit the invasion and metastasis of HepG2 and SMMC-7721 of hepatocellular carcinoma cell lines, which are related to the up-regulated expression of TIMP-3 and down-regulated expression of caveolin-1 and may be realized through the Wnt/ß-catenin signaling pathway.