Revealing the Effect of the Microstructure on Potassium Storage Behavior in a Two-Dimensional Mesoporous Carbon Anode.

Hard carbon is considered as the most promising anode material for potassium-ion energy storage devices. Substantial progress has been made in exploring advanced hard carbons to solve the issues of sluggish kinetics and large volume changes caused by the large radius of K+. However, the relationship between their complicated microstructures and the K+ charge storage behavior is still not fully explored. Herein, a series of two-dimensional mesoporous carbon microcoins (2D-MCMs) with tunable microstructures in heteroatom content and graphitization degree are synthesized by a facile hard-template method and follow a temperature-controllable annealing process. It is found that high heteroatom content makes for surface-driven K+ storage behavior, which increases the capacity-contribution ratio from a high potential region, while a high graphitization degree makes for K+ intercalation behavior, which increases the capacity-contribution ratio from a low potential region. Electrochemical results from a three-electrode Swagelok cell demonstrate that a 2D-MCM anode with more capacity contribution from a low working region allows the porous carbon cathode to be operated in a much wider electrochemical window, thus storing more charge. As a result, potassium-ion capacitors based on the optimized 2D-MCM anode deliver a high energy density of 113 Wh kg-1 and an exhilarating power density of 51,000 W kg-1.

RUNX1-induced upregulation of PTGS2 enhances cell growth, migration and invasion in colorectal cancer cells.

Colorectal cancer (CRC) arises via the progressive accumulation of dysregulation in key genes including oncogenes and tumor-suppressor genes. Prostaglandin-endoperoxide synthase 2 (PTGS2, also called COX2) acts as an oncogenic driver in CRC. Here, we explored the upstream transcription factors (TFs) responsible for elevating PTGS2 expression in CRC cells. The results showed that PTGS2 silencing repressed cell growth, migration and invasion in HCT116 and SW480 CRC cells. The two fragments (499-981 bp) and (1053-1434 bp) were confirmed as the core TF binding profiles of the PTGS2 promoter. PTGS2 expression positively correlated with RUNX1 level in colon adenocarcinoma (COAD) samples using the TCGA-COAD dataset. Furthermore, RUNX1 acted as a positive regulator of PTGS2 expression by promoting transcriptional activation of the PTGS2 promoter via the 1086-1096 bp binding motif. In conclusion, our study demonstrates that PTGS2 upregulation induced by the TF RUNX1 promotes CRC cell growth, migration and invasion, providing an increased rationale for the use of PTGS2 inhibitors in CRC prevention and treatment.

[Effects of exogenous hydrogen sulfide on pulmonary hypertension in rabbits with endotoxic shock].

Objective: To investigate the effects of exogenous hydrogen sulfide (H2S) on pulmonary vascular reactivity induced by endotoxic shock (ES) in rabbits. Methods: In this experiment, the model of endotoxic shock (ES) was induced by injection of lipopolysaccharides (LPS) to New Zealand big eared white rabbit through jugular vein (8 mg/0.8 ml/kg), the intervention was performed by H2S donor(sodium hydrosulfide, NaHS) which was injected intraperitoneally (28 µmol/kg) 15 min in advance. New Zealand rabbits were randomly divided into 4 groups(n=8):control group, LPS group, LPS+NaHS group and NaHS group. The changes of mean arterial pressure (MAP) and mean pulmonary arterial pressure (MPAP) were detected. The tension of pulmonary artery ring (PARs) was detected byin vitro vascular ring technique. The ultrastructure of pulmonary artery wall and pulmonary artery endothelial cells were observed by light microscope and scanning electron microscope. Results: ①MAP was decreased while MPAP was increased in rabbits after LPS injection, and ES animal model was established successfully. Compared with LPS group, mPAP of rabbit in LPS+NaHS group was decreased significantly (all P＜0.05). ②Compared with normal control group, pulmonary artery of rabbits in LPS group had an increased contractile response to phenylephrine (PE) and a decreased relaxation response to acetylcholine (ACh) (both P＜0.01); Compared with LPS group, pulmonary artery of rabbits in LPS+NaHS group had a decreased contractile response to PE and an increased relaxation response to ACh (both P＜0.05). ③Under light microscope, the structure of vascular endothelial cells was continuous in the normal control group, the elastic fibers were intact in the subcutaneous layer, and the smooth muscle layer was arranged neatly. LPS can shed some of the pulmonary artery endothelial cells, break the subcutaneous elastic fibers, and disorder the smooth muscle layer structure. Compared with LPS group, the injury of pulmonary artery wall in LPS+NaHS group was ameliorated. The morphology of pulmonary artery wall was normal in NaHS group. It is showed that some endothelial cells of pulmonary artery were missing in LPS group by Scanning electron microscopy. The morphology of pulmonary artery endothelial cells in LPS+NaHS group was similar to that in the control group: slightly widened intercellular space was observed, and no cell exfoliation was observed. Conclusion: These results suggest that exogenous H2S can protect pulmonary artery endothelial cells and regulate the reactivity changes of pulmonary artery during ES, which may be one of the mechanisms reducing PAH in ES rabbits.

The Toxicity and Antibacterial Effects of Povidone-Iodine Irrigation in Fracture Surgery.

OBJECTIVE: Surgical site infection is a common complication of surgery, especially in orthopedics. Povidone-Iodine (PI) is one of the oldest and most commonly used disinfectants in surgery. However, the toxicity and antimicrobial effect of PI have not been discussed. In addition, no study has explored the optimum PI concentration for sterilization and tissue healing. This study explores the germicidal efficacy of different concentrations PI, in addition, the toxicity and antibacterial effects of PI irrigation in fracture surgery are also discussed. METHODS: Methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa (P. aeruginosa) were used to evaluate the germicidal efficacy of PI in vitro and in vivo. In vitro, the effects of PI on bacterial growth were analyzed. 2.5%, 1.25%, 0.5%, 0.25%, 0.05%, 0.025%, 0.005%, 0.0025% and 0% PI was added into the bacterial suspension, besides, the bacterial algebra and growth rate were tested. Meanwhile, the fluorescence intensity of viable bacteria was also tested to evaluate the effects of PI on bacterial survival. In vivo, first, femoral fracture with wound infection rat models were established. Second, thyroid gland sections, blood thyroxine, urinary iodine, wound local skin, muscle and bone tissue sections, serum creatinine and alanine aminotransferase, serum and bone local tissue interleukin-6 (IL-6), interleukin-10 (IL-10), bone morphogenetic protein (BMP-2), vascular endothelial growth factor (VEGF) and transforming growth factor (TGF-ß1) were detected in rat femoral shaft fracture model with 5%, 2.5%, 0.5%, 0.05%, and 0% PI irrigation. Third, tissue bacteria culture was tested in rat femoral fracture with wound infection model with different concentrations PI irrigation. RESULTS: In vitro, 2.5%, 1.25%, 0.5% PI inhibited the growth of bacteria. 1.25%, 0.5% PI killed all the bacteria, while 0.25%, 0.05% PI had not killed bacteria after about 10 min. The iodine absorption of 5%, 2.5%, 0.5% PI irrigation did not cause thyroid injury. The 5%, 2.5%, 0.5% PI irrigation did not make serum creatinine and alanine aminotransferase abnormal and can remove bacteria from wounds. The 0.5%, 2.5% PI irrigation can promote tissue healing and increase BMP-2, VEGF, TGF-ß1, IL-10, in addition, decrease IL-6. 5% PI irrigation would inhibit tissue healing, and increase IL-6, decrease BMP-2, VEGF, TGF-ß1, IL-10. CONCLUSIONS: Povidone-Iodine was a widely used disinfectant and 2.5%, 1.25% and 0.5% PI could effectively kill bacteria. Five percent and lower concentration PI irrigation was safe and could not cause thyroid, kidney and liver damage. The 0.5% PI irrigation was beneficial for tissue healing but 5% PI irrigation was the opposite.

Xylomexicanins K-N: limonoids from the leaves and twigs of Xylocarpus granatum.

Six new compounds, xylomexicanins K-N (1-4), granasteroid (5) and 5-methoxy-2-pentylbenzofuran-7-ol (6), along with nine known compounds were isolated from the leaves and twigs of Xylocarpus granatum. Among them, 1 was a biogenetic precursor of 1,8,9-phragmalin limonoid, and 4 represent the first example of degraded A-ring limonoid. The structures of them were elucidated on the basis of one- and two-dimensional NMR spectroscopic data (including 1H, 13C-NMR, DEPT, 1H-1H COSY, HSQC, HMBC, and NOESY) and confirmed by high-resolution mass spectrometry.[Formula: see text].

MicroRNA-214 protects L6 skeletal myoblasts against hydrogen peroxide-induced apoptosis.

MicroRNAs (miRNAs) have been reported as key gene regulators, and they control many fundamental biological processes. Previously, we demonstrated that miR-214 had a protective effect against myocardial apoptosis and myocardial fibrosis. In this study, we sought to investigate the expression of miR-214 in L6 skeletal myoblast (SKM), the regulatory effect of miR-214 on hydrogen peroxide (H2O2) induced cell apoptosis and the underlying mechanisms of the antiapoptotic effect. MiR-214 expression was up-regulated by H2O2 in a dose and time-dependent manner in L6 SKMs. To investigate the regulatory effects of miR-214 on L6 SKM, both gain-of-function and loss-of-function approaches were applied. The results showed that miR-214 improved cell survival and inhibited cell apoptosis, and blockage of miR-214 abrogated the protective effect on cell survival and resistance to apoptosis. Phosphatase and tensin homolog (PTEN) was negatively regulated by miR-214, and PTEN inhibitor obviously reversed the effect of miR-214 blockage on enhancing cell apoptosis. In addition, miR-214 up-regulated antiapoptotic protein Bcl-2, down-regulated proapoptotic protein Bax, prevented release of cytochrome c and inhibited caspase-3 activation. In summary, H2O2-induced injury increases miR-214 expression in L6 SKM, and miR-214 contributes to the protection of L6 SKM against apoptosis via lowering PTEN and subsequently inhibiting the mitochondrial-mediated caspase-dependent apoptotic signaling pathway.

The long noncoding RNA CRAL reverses cisplatin resistance via the miR-505/CYLD/AKT axis in human gastric cancer cells.

Emerging evidence has suggested that long noncoding RNAs (lncRNAs) play an essential role in the tumorigenesis of multiple types of cancer including gastric cancer (GC). However, the potential biological roles and regulatory mechanisms of lncRNA in response to cisplatin, which may be involved in cisplatin resistance, have not been fully elucidated. In this study, we identified a novel lncRNA, cisplatin resistance-associated lncRNA (CRAL), that was downregulated in cisplatin-resistant GC cells, impaired cisplatin-induced DNA damage and cell apoptosis and thus contributed to cisplatin resistance in GC cells. Furthermore, the results indicated that CRAL mainly resided in the cytoplasm and could sponge endogenous miR-505 to upregulate cylindromatosis (CYLD) expression, which further suppressed AKT activation and led to an increase in the sensitivity of gastric cancer cells to cisplatin in vitro and in preclinical models. Moreover, a specific small molecule inhibitor of AKT activation, MK2206, effectively reversed the cisplatin resistance in GC caused by CRAL deficiency. In conclusion, we provide the first evidence that a novel lncRNA, CRAL, could function as a competing endogenous RNA (ceRNA) to reverse GC cisplatin resistance via the miR-505/CYLD/AKT axis, which suggests that CRAL could be considered a potential predictive biomarker and therapeutic target for cisplatin resistance in gastric cancer.

Transcription factor NF-κB in a basal metazoan, the sponge, has conserved and unique sequences, activities, and regulation.

Herein, we characterize transcription factor NF-κB from the demosponge Amphimedon queenslandica (Aq). Aq-NF-κB is most similar to NF-κB p100/p105 among vertebrate proteins, with an N-terminal DNA-binding domain, a C-terminal Ankyrin (ANK) repeat domain, and a DNA binding-site profile akin to human NF-κB proteins. Like mammalian NF-κB p100, C-terminal truncation allows nuclear translocation of Aq-NF-κB and increases its transcriptional activation activity. Expression of IκB kinases (IKKs) induces proteasome-dependent C-terminal processing of Aq-NF-κB in human cells, and processing requires C-terminal serines in Aq-NF-κB. Unlike NF-κB p100, C-terminal sequences of Aq-NF-κB do not inhibit its DNA-binding activity. Tissue of a black encrusting demosponge contains NF-κB site DNA-binding activity, as well as nuclear and processed NF-κB. Treatment of sponge tissue with LPS increases both DNA-binding activity and processing of NF-κB. A. queenslandica transcriptomes contain homologs to upstream NF-κB pathway components. This is first functional characterization of NF-κB in sponge, the most basal multicellular animal.

Liver Transplantation Using Right Lobe Graft With Focal Nodular Hyperplasia: Report of 2 Cases.

We described 2 cases of adult-to-adult liver transplantation using right lobe grafts donated by 2 patients suffering from focal nodular hyperplasia, the volumes of which were 360 cm3 and 220 cm3. This study was performed in compliance with the Declaration of the Helsinki. For preparation of the graft, back-table hepatic venous outflow reconstruction, including replacement of the retrohepatic inferior vena cava and bridging of hepatic segment V5/V8, was performed by using prosthetic vessel grafts. The liver grafts after subtracting the weight of focal nodular hyperplasia functioned well without serious small-for-size syndrome or graft dysfunction in spite of graft-to-recipient weight ratio less than 0.8%. This suggested the functioning of hepatocyte within focal nodular hyperplasia, which avoided graft deficiency. These 2 recipients were given not only conventional immunosuppressants (tacrolimus and mycophenolate sodium) but also anticoagulants (low molecular weight heparin and warfarin). Thrombosis of the prosthetic inferior vena cava 1 month after transplant in recipient 1 was treated by placement of intravascular stent. Biliary duct anastomotic stricture 2 weeks after transplant in recipient 2 was treated by placement of biliary stent. These 2 recipients remain well at more than 2 years post-transplant. These successful explorative cases highlight the safe use of a graft containing focal nodular hyperplasia. The partial liver resection grafts with focal nodular hyperplasia could be applied to the patients on the waiting list for liver transplantation.

Repeated exposure to the irrigative wastewater in Shijiazhuang induced precancerous lesion associated with cytochrome P450.

In the present study, the carcinogenic effects of the wastewater sample collected from the Dongming Canal in Shijiazhuang city were first detected by the rat medium-term liver bioassay. The experiment contained five groups: a negative control group, a DEN-alone group, 25% wastewater, 50% wastewater, and 100% wastewater. The body weight of rats decreased significantly as the dose increased. Morphologically, we also found that the damage of the hepatic lobule was more serious and the proliferation of liver cells was more obvious as the dose increased. In addition, we observed a significantly increased liver organ coefficient in rat. With the increase in dose, the damage of the hepatocytes was more serious, which was manifested in significantly elevated of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gammaglutamyl transfer peptide enzyme (γ-GT). And, the irrigative wastewater significantly increased GST-p in the liver of rats at both the transcriptional and translational levels dose-dependently, eventually causing precancerous lesions in the liver tissues. CYP1A1 and CYP1B1 expressions in the rat liver cells at the level of transcription and translation were also significantly increased dose-dependently. Our data clearly demonstrated that the irrigative wastewater had a carcinogenetic effect that was associated with CYP1A1 and CYP1B1. The risk of carcinogenic potential to human health might be due to joint action and accumulative effects over a long period of exposure. We can also concluded that the medium-term liver bioassay could be used as an effective method for evaluating the carcinogenicity of complex water mixtures such as irrigative wastewater.

miR-214 Down-Regulation Promoted Hypoxia/Reoxygenation-Induced Hepatocyte Apoptosis Through TRAF1/ASK1/JNK Pathway.

OBJECTIVE: This study investigated the role of miR-214 in the hepatocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury. MATERIALS AND METHODS: In vivo hepatic ischemia/reperfusion (HIR) injury, mice model and in vitro HR model were established. miR-214, TRAF1, ASK1, and JNK expression levels were detected by qRT-PCR and western blot. The apoptosis of mouse hepatocyte AML12 was detected by flow cytometry analysis. The interaction between miR-214 and TRAF1 was confirmed by dual-luciferase reporter gene assay. RESULTS: Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were elevated in HIR injury mice compared with sham mice. miR-214 expression was down-regulated in liver tissues of HIR and H/R-induced hepatocytes, whereas TRAF1, ASK1, and JNK expressions were up-regulated in HIR and H/R groups. H/R stimulation promoted the apoptosis of hepatocytes, and miR-214 overexpression inhibited the apoptosis of hepatocytes. Besides, TRAF1 was a target of miR-214 and negatively regulated by miR-214. miR-214/TRAF1 pathway involved in the modulation of H/R-induced apoptosis of hepatocytes. In vivo study proved miR-214 reduced hepatic injury of HIR mice. CONCLUSION: miR-214 overexpression reduces hepatocyte apoptosis after HIR injury through negatively regulating TRAF1/ASK1/JNK pathway.

Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats.

INTRODUCTION: Recent studies suggested that sulfur dioxide (SO2) can be produced endogenously by pulmonary vessels and attenuate acute lung injury (ALI) with vasorelaxant effects. This study was conducted to determine whether SO2 can inhibit lung inflammation and relax pulmonary arteries via inhibition of the mitogen-activated protein kinase (MAPK) pathway. MATERIAL AND METHODS: Forty-eight adult male Sprague Dawley rats (250~300 g) were randomly divided into six treatment groups: control (n = 8), control + SO2 (n = 8), control + L-aspartic acid-ß-hydroxamate (HDX) (n = 8), LPS (n = 8), LPS + SO2 (n = 8) and LPS + HDX (n = 8). RESULTS: Six hours after LPS treatment, rats exhibited elevated pulmonary artery hypertension (PAH), marked pulmonary structure injury with elevated pulmonary myeloperoxidase (MPO) activity and increased expression of intercellular adhesion molecule 1 (ICAM-1) and CD11b, along with decreased pulmonary SO2 production and reduced pulmonary aspartate aminotransferase (AAT) activity. Pretreatment with SO2 saline solution significantly reduced, while HDX (AAT inhibitor) aggravated, the pathogenesis of LPS-induced ALI. Moreover, SO2 saline solution significantly down-regulated expression of Raf-1, MEK-1 and phosphorylated ERK (p-ERK). It also prevented pulmonary hypertension in association with an up-regulated SO2/AAT pathway. However, HDX advanced pulmonary hypertension and inflammatory responses in the lung were associated with a down-regulated SO2/AAT pathway. CONCLUSIONS: Our results suggest that SO2 markedly relieved inflammatory responses, in association with Raf-1, MEK-1 and p-ERK during ALI induced by LPS. The down-regulation of the SO2/AAT pathway may be involved in the mechanism(s) of LPS-induced lung injury.

Anti-IL-20 monoclonal antibody suppresses hepatocellular carcinoma progression.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In the present study, it was observed that IL-20 mRNA and protein levels were markedly increased in the HCC tissues examined via reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. Mouse recombinant IL-20 (mIL-20) enhanced liver cancer cell proliferation, migration and invasion in vitro, while the anti-IL-20 monoclonal antibody (mAb) attenuated the effect of mIL-20, inhibiting cancer cell migration and invasion in vitro and suppressing cell growth in vitro and in vivo. This was detected by Cell Counting Kit-8, colony formation, Transwell assays and a xenograft tumor nude mouse model. Western blotting revealed that IL-20 promoted HCC progression through inducing transforming growth factor-ß and matrix metalloproteinase 9 expression and enhancing the phosphorylation of Jun N-terminal kinase and signal transducer and activator of transcription 3. The results of the present study indicated that IL-20 promotes HCC development. In addition, anti-IL-20 mAb may attenuate the effect of IL-20 and suppress liver tumorigenesis in vitro and in vivo, indicating that anti-IL-20 mAbs may potentially serve as effective therapeutic agents for HCC.

MicroRNA-873 Promotes Cell Proliferation, Migration, and Invasion by Directly Targeting TSLC1 in Hepatocellular Carcinoma.

BACKGROUND/AIMS: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and has the third highest mortality rate among all cancers. MicroRNAs are a class of endogenous, single-stranded short noncoding RNAs. The purpose of this study was to study the role of microRNA-873 in HCC. METHODS: The expression of miRNA-873 and tumor suppressor in lung cancer 1 (TSLC1) in HCC tissues and cell lines was detected by real-time quantitative RT-PCR (RT-qPCR) or western blot. A CCK-8 assay was used to examine cell proliferation; flow cytometry was used to assess the cell cycle; the Transwell migration assay was used to test for metastasis. Luciferase assays were performed to assess whether TSLC1 was a novel target of miRNA-873. RESULTS: We showed that miRNA-873 was upregulated in HCC tissues and cell lines compared with the normal control. Knockdown of miRNA-873 inhibited the growth and metastasis of HepG2 and accelerated G1 phase arrest, while overexpression of miRNA-873 had the opposite effect. The dual-luciferase reporter assays revealed that TSLC1 was a novel target of miRNA-873. Further study showed that TSLC1 was decreased in HCC tissues and cell lines. There was a negative correlation between the expression levels of TSLC1 and miRNA-873. The effect of miRNA-873 overexpression was neutralized by TSLC1. We also found that miRNA-873 activated the PI3K/AKT/mTOR signaling pathway and promoted HCC. CONCLUSIONS: Our data demonstrated that miRNA-873 promoted HCC progression by targeting TSLC1 and provided a new target for the therapy of HCC.

The mechanism of long non-coding RNA MEG3 for hepatic ischemia-reperfusion: Mediated by miR-34a/Nrf2 signaling pathway.

To investigate the function of MEG3 in hepatic ischemia-reperfusion (HIR) progress, involving its association with the level of miR-34a during hypoxia-induced hypoxia re-oxygenation (H/R) in vitro. HIR mice model in vivo was established. MEG3, miR-34a expression, along with Nrf2 mRNA and protein level were detected in tissues and cells. Serum biochemical parameters (ALT and AST) were assessed in vivo. A potential binding region between MEG3 and miR34a was confirmed by luciferase assays. Hepatic cells HL7702 were subjected to hypoxia treatment in vitro for functional studies, including TUNEL-positive cells detection and ROS analysis. MEG3, Nrf2 expression was significantly down-regulated in infarction lesion from HIR mice, as opposed to increased miR-34a production, while similar results were also observed in H/R HL7702 cells, while the above effects were reversed by MEG3 over-expression. By using bioinformatics study and RNA pull down combined with luciferase assays, we demonstrated that MEG3 functioned as a competing endogenous RNA (ceRNA) for miR-34a, and there was reciprocal repression between MEG3 and miR-34a in an Argonaute 2-dependent manner. Functional studies demonstrated that MEG3 showed positive regulation on TUNEL-positive cells and ROS level. Further in vivo study confirmed that MEG3 over-expression could improve hepatic function of HIR mice, and markedly decreased the expression of serum ALT and AST. MEG3 protected hepatocytes from HIR injury through down-regulating miR-34a expression, which could add our understanding of the molecular mechanisms in HIR injury.

lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214.

The aberrant expression of long noncoding RNAs (lncRNAs) has been involved in various human tumors including hepatocellular carcinoma (HCC). Our study aimed to investigate the potential molecular mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in HCC. The expression of MIAT and micro-RNA (miR)-214 in HCC tissues and cells was examined by quantitative real-time PCR, and the levels of enhancer of zeste homolog 2 (EZH2) and ß-catenin were detected by Western blot assay. Immunoprecipitation analysis was used to detect the level of H3/H4 histone acetylation. RNA pull-down assay was performed to confirm the targeting regulatory relationship between miR-214 and MIAT. Cell viability, proliferation, and invasion were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), [3H]thymidine incorporation, and Transwell assays, respectively. BALB/c nude mice were used to establish a hepatocellular carcinoma animal model with subcutaneous injection of SK-HEP-1 cells. Upregulation of MIAT is related to the proliferation and invasion of HCC, and downregulating MIAT expression inhibited HCC cell proliferation and invasion. The H3/H4 histone acetylation level of MIAT promoter in HCC tissues was higher than that in normal tissues. MIAT negatively regulated miR-214 in HCC cells. Inhibition of miR-214 reversed the influence of MIAT downregulation on HCC cell proliferation and invasion. In nude mouse xenograft models, downregulation of MIAT markedly suppressed the tumor growth of HCC via releasing miR-214. In conclusion, lncRNA MIAT promotes the proliferation and invasion of HCC cells through sponging miR-214, which brings a novel target for the therapy and prognosis of hepatocellular carcinoma. NEW & NOTEWORTHY This is the first research showing long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) to have a regulatory effect on hepatocellular carcinoma. Micro-RNA (miR)-214 could be sponged by MIAT to promote the proliferation and invasion of hepatocellular carcinoma cells. The lncRNA MIAT/miR-214 axis brings a novel insight for the therapy and prognosis of hepatocellular carcinoma.

Long non-coding RNA Myd88 promotes growth and metastasis in hepatocellular carcinoma via regulating Myd88 expression through H3K27 modification.

Enhanced Myd88 expression has been found in various parenchymal tumors especially in hepatocellular carcinoma with little mechanism of its upregulation known. A lot of long non-coding RNAs are reported to regulate the protein-coding genes which have location association through various mechanisms. In our study we confirmed a new long non-coding RNA Myd88 aberrant upregulated in HCC located upstream of Myd88 and verified a positive regulation relationship between them indicating that Lnc-Myd88 might participate in the enhanced expression of Myd88 in HCC. The gain- and loss-of-function analysis revealed that Lnc-Myd88 could promote the proliferation and metastasis of HCC both in vitro and in vivo. In addition, ChIP assays demonstrated that Lnc-Myd88 might increase Myd88 expression through enhancing H3K27Ac in the promoter of Myd88 gene, thus resulting in the activation of both NF-κB and PI3K/AKT signal pathways. In conclusion, we proposed that Lnc-Myd88 might serve as a novel diagnosis and therapeutic target for HCC.

Liver transplantation using the otherwise-discarded partial liver resection graft with hepatic benign tumor: Analysis of a preliminary experience on 15 consecutive cases.

RATIONALE: The shortage of available donor organs limits the development of liver transplantation. This case-serial study presents a novel way to expand the donor pool by using the other-wise discarded partial liver resection graft with hepatic benign tumor. PATIENT CONCERNS: From 2012 to 2016, 15 patients with hepatic lesions were admitted to our hospital. 12 patients suffered from right epigastric discomfort and 3 patients worried about uncertain diagnosis. INTERVENTIONS: Regular hepatic lobectomy was performed for all patients and after back-table management the resected partial liver grafts were used for patients with end-stage liver disease for liver transplantation. OUTCOMES: All patients had improved liver function within 1 week of transplantation. Patients had no serious small-for-size syndrome despite graft-to-recipient weight ratio less than 0.8%. Back-table hepatic venous reconstruction with prosthetic vascular grafts was performed without serious early complications, and late thrombosis in vessel graft did not affect liver function. Postoperative computed tomography scans demonstrated a remarkable growth in graft volume and a continuous decrease in hemangioma in recipients using the grafts with hemangioma. One patient died from pulmonary embolism on day 7 after transplant, and the rest of 14 recipients had been surviving well, especially recipient 1 for more than 4 years, although 3 recipients had tumor recurrence and had been treated with sorafenib. DIAGNOSES: The postoperative pathological diagnosis reported cavernous hemangioma (n = 11), perivascular epithelioid cell tumor (n = 2), inflammatory pseudotumor for (n = 1), and focal nodular hyperplasia (n = 1). LESSONS: The partial liver grafts with hepatic benign tumors are safe for liver transplantation. In addition, prosthetic vascular grafts can be used for hepatic venous outflow reconstruction, especially in right lobe liver transplantation.

A Meta-analysis comparing the effect of anatomical resection vs. non-anatomical resection on the long-term outcomes for patients undergoing hepatic resection for hepatocellular carcinoma.

BACKGROUND: This study aimed to compare the outcomes of patients undergoing anatomical resection (AR) versus non-anatomical resection (NAR) for hepatocellular carcinoma (HCC) from the published comparative studies within the literatures. METHODS: A meta-analysis of studies published from 2001 to 2010 were conducted using RevMan 5.0. Measured outcomes were morbidity, mortality, recurrence and 5 year overall (OS) and disease free (DFS) survival. RESULTS: Seventeen observational studies involving 3129 patients were analyzed: 1626 (52%) in AR group and 1503 (48%) in NAR group. The 5-year OS (RR, 1.18; 95% CI, 1.03-1.36; P = 0.018) and DFS (RR, 1.56; 95% CI, 1.23-1.97; P < 0.001) were significantly greater in the AR group than the NAR group, while the overall recurrence was significantly lower (RR, 0.84; 95% CI, 0.75-0.94; P < 0.001). There were no significant differences in mortality (RR, 1.00; 95% CI, 0.80-1.25; P = 0.980) or morbidity (OR, 0.97; 95% CI, 0.48-1.99; P = 0.943) between the AR and NAR groups. CONCLUSION: AR for HCC is superior to NAR considering its higher 5-year OS and DFS rates and lower overall recurrence rate. Heterogeneity detection within the analysis suggests these results should be interpreted with caution and further well designed studies are required to address this issue.

MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent.

The functional impact of recently discovered miRNAs in human cancer remains to be clarified. One miRNA in colorectal cancer which has attracted attention is miR-545. In this study, we examined the function of miR-545 in proliferation of colorectal cancer cells. Expressions of HOTAIR, miRNA-545, and epidermal growth factor receptor (EGFR) mRNA were measured in 100 paired cancerous and non-cancerous tissues as well as in SW480 and LOVO colorectal cancer cell (CRC) lines by quantitative RT-PCR. The relative protein level of EGFR was measured using western blotting. Effects of miRNA-545 and HOTAIR on gastric cancer cells were studied by overexpression and RNA interference approaches. Insight of mechanism of promotion cancer by miR-545 was gained from luciferase reporter assay and gene expression analysis. CRC proliferation was evaluated using clone formation and MTT assay. Differential expressions of HOTAIR, miR-545, and EGFR were observed in cancerous tissues in comparison to non-cancerous tissues. By expressional management of miR-545, we observed that miR-545 negatively regulated cell proliferation. Also luciferase reporter assay revealed that miR-545 inhibited regulated EGFR expression by affecting its 3'-UTR activity. In addition, miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. Monitoring of tumor growth in mice showed that miR-545 overexpression suppressed LOVO tumor growth. Our data suggested that HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.