A Flexible and Stretchable MXene/Waterborne Polyurethane Composite-Coated Fiber Strain Sensor for Wearable Motion and Healthcare Monitoring.

Fiber-based flexible sensors have promising application potential in human motion and healthcare monitoring, owing to their merits of being lightweight, flexible, and easy to process. Now, high-performance elastic fiber-based strain sensors with high sensitivity, a large working range, and excellent durability are in great demand. Herein, we have easily and quickly prepared a highly sensitive and durable fiber-based strain sensor by dip coating a highly stretchable polyurethane (PU) elastic fiber in an MXene/waterborne polyurethane (WPU) dispersion solution. Benefiting from the electrostatic repulsion force between the negatively charged WPU and MXene sheets in the mixed solution, very homogeneous and stable MXene/WPU dispersion was successfully obtained, and the interconnected conducting networks were correspondingly formed in a coated MXene/WPU shell layer, which makes the as-prepared strain sensor exhibit a gauge factor of over 960, a large sensing range of over 90%, and a detection limit as low as 0.5% strain. As elastic fiber and mixed solution have the same polymer constitute, and tight bonding of the MXene/WPU conductive composite on PU fibers was achieved, enabling the as-prepared strain sensor to endure over 2500 stretching-releasing cycles and thus show good durability. Full-scale human motion detection was also performed by the strain sensor, and a body posture monitoring, analysis, and correction prototype system were developed via embedding the fiber-based strain sensors into sweaters, strongly indicating great application prospects in exercise, sports, and healthcare.

Poly(ether imide) Porous Membrane Developed by a Scalable Method for High-Performance Lithium-Sulfur Batteries: Combined Theoretical and Experimental Study.

Lithium-sulfur (Li-S) batteries are one of the emerging candidates for energy storage systems due to their high theoretical energy density and the abundance/nontoxicity/low cost of sulfur. Compared with conventional lithium-ion batteries, multiple new challenges have been brought into this advanced battery system, such as polysulfide shuttling in conventional polyolefin separators and undesired lithium dendrite formation of the Li metal anode. These issues severely affect the cell performance and impede their practical applications. Herein, we develop a poly(ether imide) (PEI)-based membrane with a sponge-like pore morphology as the separator for the Li-S battery by a simplified phase inversion method. This new separator can not only alleviate the new challenges in Li-S batteries but also exhibit excellent ion conductivity, better thermal stability, and higher mechanical strength compared to those of the conventional polypropylene (PP) separator. A combined experimental and theoretical study indicates that the sponge-like morphology of the PEI membrane and its good wettability toward the electrolyte can facilitate uniform ion transportation and suppress dendrite growth. Meanwhile, the PEI molecules exhibit a strong interaction with polysulfides and avoid their shuttling effectively. As a result, the PEI-based Li-S battery shows a much better performance from various aspects (capacity, rate capability, and cycling stability) than that of the PP-based Li-S battery, especially at high charge/discharge current densities and high sulfur loadings. Since the developed PEI membrane can be easily scaled up, this work may accelerate the practical applications of Li-S batteries from the point of separators.

Exosomes: A New Pathway for Cancer Drug Resistance.

Exosomes are extracellular vesicles (EVs) that are secreted into body fluids by multiple cell types and are enriched in bioactive molecules, although their exact contents depend on the cells of origin. Studies have shown that exosomes in the tumor microenvironment affect tumor growth, metastasis and drug resistance by mediating intercellular communication and the transport of specific molecules, although their exact mechanisms of action need to be investigated further. In this review, we have summarized current knowledge on the relationship between tumor drug resistance and exosomes, and have discussed the potential applications of exosomes as diagnostic biomarkers and therapeutic targets.

Mid-term Results of Coil Embolization Alone and Stent-assisted Coil Embolization for Renal Artery Aneurysms.

BACKGROUND: Coil embolization (CE) alone and stent-assisted coil embolization (SCE) are two major endovascular techniques to treat renal artery aneurysms (RAAs). This study aimed at providing safety and efficacy data of CE and SCE for RAAs. METHODS: Between August 2015 and June 2019, 40 RAA patients treated with CE or SCE were included in the retrospective study. Patients' demographics, clinical manifestations, aneurysm characteristics, treatment strategies, and follow-up results were collected and analyzed. RESULTS: There were 26 and 14 patients in the CE and SCE group, respectively. The mean aneurysm diameter was 2.5 ± 1.5 cm and 2.2 ± 0.8 cm (CE versus SCE, P = 0.52). The neck width of the aneurysm was 0.63 ± 0.37 cm and 1.07 ± 0.42 cm (CE versus SCE, P = 0.021). Technical success was achieved in 97.5% patients. No death or aneurysm rupture occurred. During the perioperative period, 12% and 7.1% patients suffered partial renal infarction (CE versus SCE, P = 0.45). The mean duration of follow-up was 8.8 ± 9.4 months and 16.1 ± 16.3 months (CE versus SCE, P = 0.158) by imaging and 20.8 ± 11.3 and 22.7 ± 16.5 months by visit/telephone (CE versus SCE, P = 0.703). During the follow-up, 17.4% patients in the CE group and 30.8% patients in the SCE group suffered partial renal infarction, while their overall renal function remained normal. In addition, there was no aneurysm recurrence, sac enlargement, or death in both groups. CONCLUSIONS: Both CE and SCE were safe and effective to treat RAAs. In addition, SCE may prevent coil migration in the wide neck aneurysm in selected patients.

Novel homozygous mutations in PATL2 lead to female infertility with oocyte maturation arrest.

PURPOSE: To identify the disease gene in 40 patients with female infertility due to oocyte maturation arrest. METHODS: Genomic DNA was extracted from peripheral blood of 40 patients and their family members. Whole-exome sequencing was performed on the patients, and the PATL2 mutations were identified and confirmed by Sanger sequencing. Harmfulness of the mutations was analyzed by SIFT, Polyphen-2, Mutation Taster, and M-CAP software, and we used western immunoblotting analysis to check the effect of mutations on PATL2 protein expression in vitro. RESULTS: Two novel missense mutations c.1528C>A (p.Pro510Thr) and c.1376C>A (p.Ser459Tyr) in PATL2 were identified in three patients (7.5%) from two consanguineous families in our cohort. We found that mutations in PATL2 resulted in variable oocyte phenotypes, including GV arrest, MI arrest, and morphologic abnormalities. Western immunoblotting analysis showed that the expression levels of the two novel mutant PATL2 proteins decreased significantly. CONCLUSIONS: We identified two novel PATL2 mutations that caused oocyte maturation arrest and abnormal morphology, and variable phenotypes in patients.

The Difference Se Makes: A Bio-Inspired Dppf-Supported Nickel Selenolate Complex Boosts Dihydrogen Evolution with High Oxygen Tolerance.

Inspired by the metal active sites of [NiFeSe]-hydrogenases, a dppf-supported nickel(II) selenolate complex (dppf=1,1'-bis(diphenylphosphino)ferrocene) shows high catalytic activity for electrochemical proton reduction with a remarkable enzyme-like H2 evolution turnover frequency (TOF) of 7838 s-1 under an Ar atmosphere, which markedly surpasses the activity of a dppf-supported nickel(II) thiolate analogue with a low TOF of 600 s-1 . A combined study of electrochemical experiments and DFT calculations shed light on the catalytic process, suggesting that selenium atom as a bio-inspired proton relay plays a key role in proton exchange and enhancing catalytic activity of H2 production. For the first time, this type of Ni selenolate-containing electrocatalyst displays a high degree of O2 and H2 tolerance. Our results should encourage the development of the design of highly efficient oxygen-tolerant Ni selenolate molecular catalysts.

A square-planar nickel dithiolate complex as an efficient molecular catalyst for the electro- and photoreduction of protons.

A square-planar nickel(ii) dithiolate complex is an active molecular catalyst for both photoreduction of protons from water with a turnover number (>1500) and electroreduction of protons from weakly acidic solutions with remarkable turnover frequencies (5575 s-1 at -1.92 V and 1441 s-1 at -1.61 V vs. SCE). DFT calculations provide in-depth insight into the catalytic cycle of the electrochemical reaction, suggesting that the sulfur atoms play crucial roles in proton exchange and hydrogen formation.

YMO1 suppresses invasion and metastasis by inhibiting RhoC signaling and predicts favorable prognosis in hepatocellular carcinoma.

Previous studies have shown that 4.1 proteins, which are deregulated in many cancers, contribute to cell adhesion and motility. Yurt/Mosaic eyes-like 1 (YMO1) is a member of 4.1 protein family but it is unclear whether YMO1 plays a role in tumor invasion. This study aimed to investigate the effects of YMO1 on hepatocellular carcinoma (HCC) and attempted to elucidate the underlying molecular mechanisms. YMO1 expression in HCC tissues and its correlation with clinicopathological features and postoperative prognosis was analyzed. The results showed that YMO1 was down-regulated in the highly metastatic HCC cell line and in human tumor tissues. Underexpression of YMO1 indicated poor prognosis of HCC patients. Restoration of YMO1 expression caused a significant decrease in cell migration and invasiveness in vitro. In vivo study showed that YMO1 reduced liver tumor invasion and metastasis in xenograft mice. YMO1 directly inhibited RhoC activation. YMO1 expression in HCC was regulated by PAX5. Analysis of YMO1 expression levels in human HCC patients revealed a significant correlation of YMO1 expression with PAX5 and RhoC. Our findings revealed that YMO1 predicts favorable prognosis and the data suggest that YMO1 suppresses tumor invasion and metastasis by inhibiting RhoC activity.

[Effects of Down-regulating PPP2R5C Expression on Expression Profile of TAL1-related Regulating Genes in Jurkat Cells].

OBJECTIVE: Based on our previous study showing the inhibition of lenkemia T cell proliferation by down-regulating PPP2R5C expression, this study was aimed to analyze the influence of down-regulating PPP2R5 expression via RNA interference on genes relatied with TAL1 signaling pathway by using gene chip technique. METHODS: The PPP2R5C-siRNA799 was transduced into Jurkat cells by nucleofection, the total RNA was isolated from treated Jurkat cells after culture for 48 hours; the target sequences were prepared by revevse transcription after mRNA purification, and were hybridized with affymetrix gene expression profile chip 3' IVT. The original image data were collected using affymetrix gene chip scanner 3 000, and the gene expression profile was analyzed using gene spring GX 11.0 soflware. RESULTS: The expression of all 26 genes related with TAL1 signaling pathway was changed, out of which the expression of 15 genes were up-regulated and the expression of 11 genes was down-regulated in PPP2R5C-siRNA 799-transfected Jurkat cells. The genes with significantly up-regulated expression were GATA1, TCF4, XRCC6 and TCF3, while the genes with significantly down-regulated expression were SIN3A and RUNX1. CONCLUSION: The down-regulation of PPP2R5C gene expression in Jurkat cells via RNA interference to a certain degree can inhibit TAL1 signaling pathway genes, thereby suppresses the proliferation of Jurkat cells.

Epidermal growth factor-like domain-containing protein 7 (EGFL7) enhances EGF receptor-AKT signaling, epithelial-mesenchymal transition, and metastasis of gastric cancer cells.

Epidermal growth factor-like domain-containing protein 7 (EGFL7) is upregulated in human epithelial tumors and so is a potential biomarker for malignancy. Indeed, previous studies have shown that high EGFL7 expression promotes infiltration and metastasis of gastric carcinoma. The epithelial-mesenchymal transition (EMT) initiates the metastatic cascade and endows cancer cells with invasive and migratory capacity; however, it is not known if EGFL7 promotes metastasis by triggering EMT. We found that EGFL7 was overexpressed in multiple human gastric cancer (GC) cell lines and that overexpression promoted cell invasion and migration as revealed by scratch wound and transwell migration assays. Conversely, shRNA-mediated EGFL7 knockdown reduced invasion and migration. Furthermore, EGFL7-overexpressing cells grew into larger tumors and were more likely to metastasize to the liver compared to underexpressing CG cells following subcutaneous injection in mice. EGFL7 overexpression protected GC cell lines against anoikis, providing a plausible mechanism for this enhanced metastatic capacity. In excised human gastric tumors, expression of EGFL7 was positively correlated with expression levels of the mesenchymal marker vimentin and the EMT-associated transcription repressor Snail, and negatively correlated with expression of the epithelial cell marker E-cadherin. In GC cell lines, EGFL7 knockdown reversed morphological signs of EMT and decreased both vimentin and Snail expression. In addition, EGFL7 overexpression promoted EGF receptor (EGFR) and protein kinase B (AKT) phospho-activation, effects markedly suppressed by the EGFR tyrosine kinase inhibitor AG1478. Moreover, AG1478 also reduced the elevated invasive and migratory capacity of GC cell lines overexpressing EGFL7. Collectively, these results strongly suggest that EGFL7 promotes metastasis by activating EMT through an EGFR-AKT-Snail signaling pathway. Disruption of EGFL7-EGFR-AKT-Snail signaling may a promising therapeutic strategy for gastric cancer.

A simple BODIPY-aniline-based fluorescent chemosensor as multiple logic operations for the detection of pH and CO2 gas.

A simple 4-aniline boron-dipyrromethene (BODIPY) dye (1) was developed as a highly sensitive acidic pH fluorescent probe excitable with visible light based on a photoinduced electron transfer (PeT) mechanism. The pH titration indicates that the fluorescence intensity increases more than 500-fold within the pH range of 4.12-1.42 with a pKa value of 3.24 in methanol-water (1 : 1, v/v) solution, which is valuable for studying strongly acidic conditions. Density functional theory (DFT) calculations reproduce the fluorescence off-on behavior. 1 has also been used as a fluorescent chemosensor for the visual detection of dissolved carbon dioxide (CO2) gas. The underlying mechanism of the sensing process is rationalized. This probe can be recovered by bubbling nitrogen (N2) gas into CO2-treated solutions for over 10 cycles. In addition, two logic gates (OR and INH) have been achieved at the molecular level by changing the initial states of system 1 and chemical inputs.

[Overexpression of eIF4E gene in acute myeloid leukemia and its relation with disease progression].

The aim of this study was to detect the expression level of eIF4E gene in patients with non-treated, remission and non-remission/relapse acute myeloid leukemia (AML), and other non-malignant haematologic diseases so as to analyze and reveal the relationship of eIF4E gene expression with AML progression. SYBR Green I RT-PCR was used to assay the expression level of eIF4E mRNA extracted from bone marrow mononuclear cells in 30 patients with AML (6 in M2, 5 in M3, 8 in M4, 10 in M5, 1 in M6) and 20 patients with non-malignant hematologic diseases. The ß2-microglubin(ß2M) was used as internal reference and the formula 2(-ΔCt)×100% was applied to calculate the expression level of eIF4E gene. The results showed that the eIF4E expression level (7.098 ± 5.544)% in patients with non-treated and non-remitted/relapsed AML was significantly higher than that in patients with remission (0.964 ± 0.312)% (P < 0.01) and non-malignant hematologic diseases (0.248 ± 0.163)% (P < 0.01). There was no difference between latter two group patients, even though the expression level of eIF4E gene in patients with M4 and M5 was higher. As compared with non-malignant hematologic diseases, the expression level of eIF4E gene of patients with remission patients showed no significant difference. It is concluded that the over-expression of eIF4E gene has been found in patients with AML, and its level obviously decreases along with remission of disease, thus the eIF4E gene may be a surveillance parameter for disease progression.

Expression of C-X-C chemokine receptor types 1/2 in patients with gastric carcinoma: Clinicopathological correlations and significance.

C-X-C chemokine receptor types 1/2 (CXCR1/2) may play multiple roles in the development and progression of a number of types of tumor. The abnormal expression of CXCR1/2 in various types of malignant tumors has been reported, but less is known with regard to gastric carcinoma. The present study was preliminarily conducted to elucidate the correlation between clinicopathological factors and the immunohistochemical expression of CXCR1/2 in patients with gastric carcinoma. The expression of CXCR1/2 in 69 specimens of sporadic gastric carcinoma and their corresponding non-neoplastic mucosa obtained by gastrectomy was assayed by immunohistochemistry (IHC) using a polyclonal anti-CXCR1/2 antibody. ERK1/2 and AKT phosphorylation and the expression of indicators of proliferation, growth and apoptosis (Bcl-2 and Bax, Cyclin D1, EGFR and Ki-67), angiogenesis (VEGF and CD34), invasion and metastasis (MMP-9, MMP-2, TIMP-2 and E-cadherin) were also detected by IHC. A total of 68 (98.6%) of the 69 patients with gastric carcinoma were found to have positive CXCR1/2 expression, which appeared to be significantly higher in gastric carcinoma compared with corresponding non-neoplastic mucosa tissues. The expression of CXCR1/2 in gastric carcinoma was significantly associated with invasion, metastasis and TNM staging (P<0.001). Correlation analysis between CXCR1/2 and pAKT (P=0.032), pERK (P<0.001), Cyclin D1 (P=0.049), EGFR (P=0.013), Bcl-2 (P=0.003), microvessel density (P=0.001), MMP-9 (P=0.013) and MMP-2 (P=0.027) expression using the Spearman test showed significant correlation in gastric carcinoma. Univariate and multivariate logistic regression analysis showed that, compared with negative or weak expression, overexpression of CXCR1/2 protein was a significant risk factor for TNM stage (P<0.001). These results preliminarily suggest that CXCR1/2 may be a useful maker for progression of the tumors and a promising target for gastric carcinoma therapy.

Upregulation of C-X-C chemokine receptor type 1 expression is associated with late-stage gastric adenocarcinoma.

Chemokine receptors play multiple roles in the development and progression of various tumor types. The aim of this study was to examine C-X-C chemokine receptor type 1 (CXCR1) protein expression in gastric adenocarcinoma and to investigate the clinical implications of CXCR1 upregulation. Expression of CXCR1 protein in 83 specimens of sporadic gastric adenocarcinoma and their corresponding non-neoplastic mucosa obtained by gastrectomy was assayed using immunohistochemistry. The intensity of immunostaining in tumor tissue was considered strong when tumor tissue staining was more intense than in the corresponding non-neoplastic mucosa; the intensity was null when staining was weaker in the tumor than in the corresponding non-neoplastic mucosa; and the intensity was weak when staining was similar in both tissues. Microvascular density in tumor tissue and its corresponding non-neoplastic mucosa was measured using monoclonal antibody against CD34. A strong correlation was observed between elevated CXCR1 protein expression and tumor stage (P<0.05). T stage, N stage and overall stage positively correlated with CXCR1 protein expression. Microvascular density was higher in tumors with strong CXCR1 protein expression, but the correlation with CXCR1 was not linear (P=0.07). Multiple logistic regression analyses showed that, compared to no or weak expression, overexpression of CXCR1 protein was a significant risk factor for high N stage (N2, N3). These results indicate that CXCR1 may be considered as a new and promising target for gastric adenocarcinoma therapy.

Activator protein-1 involvement in proliferation inhibition by gene silencing of Twist in gastric cancer cells.

AIMS: To study the role of the Twist gene in growth of gastric cancer cell line MKN45 and the possible mechanisms involved. METHODS: Human gastric carcinoma MKN45 cells were stably transfected with Twist antisense plasmid using the lipofectamine transfection technique. Expression of Twist in Twist antisense plasmid transfected cells (TwistAS), non-transfected cells (NT) and non-specific Twist antisense plasmid transfected cells (CON) were examined by Western blotting. Cell growth ability in vitro was evaluated by MTT and clone formation assays. Xenograft cancer models were established by nude mouse transfer method. Activator protein-1 (AP-1) DNA binding activity was measured by electrophoretic mobility shift assay (EMSA). The expression of c-Jun and c-Fos were examined by Western blotting. The mRNA level of cyclin D1 was detected by RT-PCR. RESULTS: TwistAS inhibited cell growth and proliferation. In vitro, the cloning efficiency of TwistAS cells (8.0  ±  0.6%) was significantly lower compared to that in NT (26.5  ±  1.1%) and CON (22.7  ±  1.2%). In vivo, the average tumour weight was lighter in the TwistAS group (425.3  ±  20.8  mg) compared with the CON group (1217.0  ±â€Š 50.2  mg) and the NT group (1120.6  ±â€Š 75  mg). TwistAS inhibited AP-1 activity in MKN45 cells (15.3  ±  3.2% versus 50.2  ±â€Š 3.6% and 52.4  ±  3.8%). TwistAS inhibited the expression of c-Fos in MKN45 cells (20.4  ±  3.8% versus 72.5  ±  3.6% and 75.3  ±â€Š 4.0%) but not c-Jun (p < 0.05). cyclin D1 mRNA level was significantly lower in TwistAS cells (40.5  ±  3.8%) than that in CON (132  ±â€Š 5.4%) and NT cells (130  ±  5.2%). CONCLUSIONS: This study demonstrated that down-regulation of the Twist gene suppressed the proliferation of MKN45 gastric cancer cells by negatively regulating the AP-1 activity resulting in the cyclin D1 mRNA level decreasing.

Transplantation of human Wharton's Jelly-derived stem cells alleviates chemically induced liver fibrosis in rats.

There is currently no effective treatment method available for liver fibrosis. We therefore evaluated the use of Wharton's jelly stem cells (WJSCs; the major umbilical cord stem cell population) to treat chemically induced liver fibrosis via intraperitoneal injection of thioacetamide. WJSCs were transplanted into liver-damaged rats via the portal vein and the treatment was evaluated by assessing serum biochemistry and histopathology. Transplanted WJSCs were distributed in the fibrotic area and around blood vessels, and hepatic recovery was accelerated. Serum prothrombin time significantly recovered, and serum albumin also improved at 21 days posttransplantation; collagen accumulation also decreased at 14 days. Thus, human WJSCs promoted recovery after chronic liver damage. Using immunohistochemical analyses, we determined that transplanted WJSCs produce albumin, hepatocyte growth factor (HGF), and metalloproteinase (MMP) after transplantation to chemically injured liver, indicating that WJSC may help to decrease liver collagen and thus may be useful for treating liver fibrosis.

Reduced stratifin expression can serve as an independent prognostic factor for poor survival in patients with esophageal squamous cell carcinoma.

UNLABELLED: Stratifin plays an important role in cancer biology by interfering with intracellular signalling pathways and cell-cycle checkpoints. Decreased expression of stratifin gene has been reported to be a poor prognostic indicator in a variety of human malignant tumors. AIM: To clarify the role and prognostic significance of stratifin in esophageal squamous cell carcinoma (ESCC). METHODS: The alteration of stratifin messenger RNA (mRNA) and protein was analyzed by reverse-transcription and quantitative real-time polymerase chain reaction (QRT-PCR) and Western blotting in 20 paired ESCC and nonneoplastic esophageal mucosa tissues, respectively. Then, immunohistochemistry (IHC) was used to evaluate expression of stratifin in tissues of 148 ESCC patients (including the former 20 pairs of tissues) and correlate it with clinicopathological parameters and prognosis of ESCC patients. RESULTS: The stratifin level of mRNA and protein was markedly downregulated in ESCC tissue compared with in corresponding nonneoplastic esophageal epithelium (P<0.05). Similarly, the positive rate of stratifin protein expression was lower in the esophageal cancer than in paired nonneoplastic esophageal epithelium as detected by IHC (P=0.007). Statistically, the downregulation of stratifin expression was correlated with tumor infiltration depth (P=0.003), lymph node metastasis (P=0.008), distant metastasis (P=0.013), and lymphovascular invasion (P=0.007) of ESCC. Furthermore, the reduced stratifin expression was associated with shorter 5-year survival rate of ESCC patients after curative surgery (P<0.0001). On the basis of univariate and multivariate Cox regression analysis, we found that reduced stratifin expression, T4 stage, lymph node metastasis, and distant metastasis were independent risk factors for worse prognosis in ESCC patients. CONCLUSION: The present report indicates that stratifin could be a useful indicator for prognosis of this disease, as well as a potential target for more effective therapy.

Knockdown of fascin1 expression suppresses the proliferation and metastasis of gastric cancer cells.

AIMS: Our current investigation attempts to study the role of the fascin1 gene in growth and metastasis of gastric cancer cell line MKN45. METHODS: Small interfering RNA (siRNA) was used to inhibit fascin1 expression in the human gastric cancer cell line MKN45. Expression of fascin1 in fascin1 siRNA transfected cells (sifascin1), non-transfected cells (NT) and non-specific fascin1 siRNA cells (CON) were examined by Western blotting and reverse transcription polymerase chain reaction (RT-PCR). Cell growth ability in vitro was evaluated by MTT and clone formation assays. Cell mobility in vitro was examined by the Boyden chamber assay. Nude mice metastasis models were established by abdominal cavity transfer method. Tumour growth was evaluated by immunohistochemistry with proliferating cell nuclear antigen (PCNA). RESULTS: Knockdown of fascin1 expression in MKN45 cells resulted in decreased cellular proliferative and migratory abilities. In vitro, the cloning efficiency of siFascin1 cells (34.2%) was significantly lower compared to that in NT (78.5%) (p < 0.05). The migration rate in siFascin1 cells was significantly decreased (33.7%) compared with NT cells (89.4%) (p < 0.05). In vivo, the cell proliferation rate was lower in siFascin1 cells (25.8%) compared to that in NT (75.0%) (p < 0.05). The number of tumour clones in the liver was significantly lower in siFascin1 cells (2.0 +/- 1.1) compared to that in NT (5.1 +/- 1.6) (p < 0.05). CONCLUSIONS: Our study demonstrates that down-regulation of fascin1 suppresses the proliferation and migration of gastric cancer cells MKN45, suggesting that fascin1 siRNA may offer a novel potential gene therapy approach for human gastric cancer with fascin1 over-expression.

Mesenchymal stem cells facilitate recovery from chemically induced liver damage and decrease liver fibrosis.

AIMS: To investigate the feasibility and mechanism of liver damage repair using human bone marrow mesenchymal stem cells (hBMMSCs), we investigated the potential for hBMMSCs in recovery from liver damage, including fibrotic liver repair, using the CCl(4)-induced model for liver damage in the rat. MAIN METHODS: Rats were injected with 0.5 ml/kg CCl(4) to induce liver damage and progressive liver fibrosis. hBMMSCs labeled with GFP were injected into the rats through the portal vein. KEY FINDINGS: After one day of transplantation, GFP-labeled cells were found around the liver lobules, the hepatic blood vessels, and the edge of the liver lobes. Biochemical and histopathological analyses showed significantly increased recovery from liver damage in the transplanted group. In addition, transplanted hBMMSCs express matrix metalloproteinases (MMP), and liver fibrosis was significantly decreased. The degree of fibrosis reduction paralleled the number of hBMMSCs observed in liver sections. SIGNIFICANCE: Our data suggest that hBMMSCs may facilitate recovery from chronic liver damage and may decrease liver fibrosis. Therefore, hBMMSCs are a potential option for treatment of liver cirrhosis.

Effect of pulsed electromagnetic field on the proliferation and differentiation potential of human bone marrow mesenchymal stem cells.

Pulsed electromagnetic fields (PEMFs) have been used clinically to slow down osteoporosis and accelerate the healing of bone fractures for many years. The aim of this study is to investigate the effect of PEMFs on the proliferation and differentiation potential of human bone marrow mesenchymal stem cells (BMMSC). PEMF stimulus was administered to BMMSCs for 8 h per day during culture period. The PEMF applied consisted of 4.5 ms bursts repeating at 15 Hz, and each burst contained 20 pulses. Results showed that about 59% and 40% more viable BMMSC cells were obtained in the PEMF-exposed cultures at 24 h after plating for the seeding density of 1000 and 3000 cells/cm2, respectively. Although, based on the kinetic analysis, the growth rates of BMMSC during the exponential growth phase were not significantly affected, 20-60% higher cell densities were achieved during the exponentially expanding stage. Many newly divided cells appeared from 12 to 16 h after the PEMF treatment as revealed by the cell cycle analysis. These results suggest that PEMF exposure could enhance the BMMSC cell proliferation during the exponential phase and it possibly resulted from the shortening of the lag phase. In addition, according to the cytochemical and immunofluorescence analysis performed, the PEMF-exposed BMMSC showed multi-lineage differentiation potential similar to the control group.