This study compared the microleakage of teeth restored with nine frequently used commercial dowel systems in vitro. There were significant differences between the FRC dowels and the stainless steel dowels, and even among the FRC dowel groups. As such, the hypothesis tested, which stated there are no significant differences in microleakage between teeth restored with FRC dowels and those restored with stainless

steel dowels, is rejected. Similarly, Usumez et al reported better relative microleakage results for glass and polyethylene fiber-reinforced dowel groups than for metallic and zirconia dowel groups.[14] The literature reports various leakage measurement methods, such as dye or tracer molecule penetration measurement, evaluation of bacterial this website penetration, spectrometry of radioisotopes, gas chromatography, and fluid filtration, but there is no consensus buy Lapatinib on the reliability and precision of these methods. The fluid filtration method was first described by Derkson et al[16] and then modified and used by

Pashley et al[17] to evaluate the leakage of temporary filling materials. With this method, quantitative rather than qualitative results could be obtained, and the method allows the researcher to make repeated measurements at different time intervals owing to the nondestructive design of the method. It is reported that the presence of trapped air and fluids in the microgaps at the bonding interface negatively affects the penetration

and diffusion of dyes, tracer molecules, bacteria, or ions when using the penetration evaluation methods.[18, 19] The MCE use of positively pressurized water in the fluid filtration method ensures that these kinds of difficulties are overcome.[20] Several authors reported that fluid filtration method is a more reliable and precise method than penetration measurement methods.[20, 21] As mentioned before, one of the goals of a dowel application is to reseal the prepared root canal by a proper dowel cementation process to avoid microleakage of bacteria and bacterial byproducts.[3] However, none of the dowel systems tested in this study provided an absolute seal. The percentage of the relative microleakage of pressurized water through the root canal ranged from 3.55 × 10−4% to approximately two times higher (7.06 × 10−4%) among the different groups. Test parameters in the current study were designed to standardize the resin cement and root canal surface conditioning procedures; therefore, it must be considered that differences in microleakage among the groups originated from microleakage through the dowel/cement interface.

Animals were housed on a 12-hour light/dark cycle and were provided with mice chow and water ad libitum. Experimental animal protocols and animal procedures complied with the Guide for the Care and Use of Laboratory Animals (National Academy of Sciences, NIH Publication 86-23, revised 1996) and were approved by local regulatory authorities. BAY 54-9085 (sorafenib tosylate) (Bayer HealthCare Pharmaceuticals, Montville, NJ) 30 mg/kg/day or its vehicle (Cremophor/ ethanol/ distilled water) was administered by gavage. The dosing volume used was 0.1 mL/10 g body weight. The proportions of Cremophor/ ethanol/ distilled water were 12.5% Cremophor, 12.5% ethanol, and 75% distilled water.

For the animals receiving sorafenib, the drug was first dissolved in a 50% Cremophor

/ 50% ethanol mixture and water was then added to reach JQ1 in vivo the final volume. Animals treated with the vehicle only received the analog fluid mixture without the drug. Cremophor EL was purchased from Sigma (Sigma Cat. No. C-5135). Animals were divided into three groups and their controls. For the first Vemurafenib mouse group, treatment was started 14 days before 2/3 hepatectomy and stopped 1 day before surgery; the second group received continuous sorafenib treatment beginning 14 days prior to surgery until the time of harvest; and the third group started treatment the day after 2/3 hepatectomy. Two-thirds hepatectomy was performed according to the method described by Higgins and Anderson.13 Under isoflurane anesthesia the left lateral and medchemexpress median lobes were ligated and resected. The abdominal muscular and skin walls were sutured separately with nonabsorbable material until harvesting. Animals were euthanized with Nembutal (50 mg/kg intraperitoneal) 24, 72, and 120 hours after partial hepatectomy for the first two groups and at 72 and 120 hours for the third group starting sorafenib after

surgery; liver, scar tissue, and blood samples were taken at endpoints (n = 7-14 animals/group). Liver regeneration was determined as the ratio of liver weight (g) at harvesting time/liver weight (g) at the time of partial hepatectomy. Liver weight at the time of hepatectomy was calculated using five animals sacrificed for this purpose. At harvesting time, liver sections were fixed in 10% buffered formalin and processed for staining with hematoxylin and eosin or for immunohistochemistry. The remaining liver was snap-frozen in liquid nitrogen and kept at −80°C until further use. For determination of hepatocyte proliferation, 1 mg bromodeoxyuridine (BrdU) was injected intraperitoneally 2 hours before sacrifice and BrdU incorporation was measured using the BrdU In-Situ Detection kit obtained from BD Pharmingen (BD Biosciences, San Jose, CA). BrdU incorporation was expressed as number of BrdU-positive nuclei/mm2.

“
“The diagnosis and management of bleeding disorders

is made difficult by the complexity and variety of disorders, clinical symptoms and bleeding type and severity. von Willebrand disease (VWD) and platelet disorders are disorders of primary haemostasis and together represent the most common inherited bleeding disorders. In this article, we describe the diagnosis of VWD and platelet disorders and the treatment options for VWD. The diagnosis and management of von Willebrand disease (VWD) remains problematic for many laboratories and clinicians [1]. VWD arises from deficiency and/or defects of von Willebrand factor (VWF), a multimeric adhesive signaling pathway plasma protein essential for effective primary haemostasis. VWF is a multifunctional protein [2], which explains the heterogeneity in clinical symptoms and bleeding risk, as well as diagnostic challenges. Inherited platelet disorders include abnormalities of both number and function. Our understanding of specific

rare platelet disorders has improved significantly in the last decade with the identification of specific disease-causing mutations. However, the investigation of individual patients with mild/moderate platelet disorders remains a challenge, as diagnostic tools available in most clinical laboratories often do not provide a definitive diagnosis. Improving selleckchem our ability to define the abnormalities in common platelet disorders is our next challenge. The most recent classification scheme from the International Society on Thrombosis and Haemostasis recognizes six subtypes of VWD [3]. Type 1 represents a partial quantitative deficiency of a functionally normal VWF protein. Type 3 VWD represents a severe (complete)

deficiency of VWF. Type 2 VWD represents a group of qualitative VWF defects that comprise (i) type 2A VWD [loss of high molecular weight (HMW) VWF], type 2B VWD (enhanced functional binding of VWF to platelets that typically leads to loss of HMW VWF and mild thrombocytopenia), (iii) 2N VWD (loss of VWF-FVIII binding) and (iv) 2M VWF (VWF dysfunction not associated with loss of HMW VWF). The proper identification of VWD and its type is important as it has therapeutic implications [4]. In practice, VWD and its type can be determined by a process of laboratory testing that encompasses a comprehensive 上海皓元 panel of different tests [1, 5, 6] (Table 1). The two main tests employed by virtually all laboratories are VWF antigen (VWF:Ag) and FVIII coagulant (FVIII:C); these, respectively, measure the level of VWF protein and FVIII activity. The most common VWF activity based test is the ristocetin cofactor (VWF:RCo) assay, which essentially measures VWF binding to the platelet VWF receptor GPIb. An additional test used by a proportion of laboratories is the collagen binding (VWF:CB) assay; collagen is a sub-endothelial matrix component which binds VWF in vivo.

30-32 Furthermore, this HBV DNA threshold and the duration of follow-up correspond with the definition of response to peginterferon therapy according to the recent European guidelines and the pivotal studies on peginterferon in CHB, respectively.10, 20, 33 The large majority of our patients were of Caucasian

origin and were infected with HBV genotypes A and D. Responsiveness to interferon-based therapy appears to be lower in patients with genotype Fludarabine mouse D versus patients with other genotypes, and this may explain the limited efficacy of peginterferon in our study population.9, 10, 26, 34 A recent retrospective analysis of 264 HBeAg-negative patients treated with peginterferon alfa-2a alone or in combination with lamivudine

reported that pretreatment HBsAg levels varied according to SAHA HDAC in vivo the genotype. The highest concentrations were found in patients infected with genotypes A and D. Although serum HBsAg levels decreased during the treatment phase for all genotypes, the HBsAg decline was least pronounced in patients with genotype D.35 Therefore, our data on the decline in HBsAg levels need to be confirmed in patients with genotypes B and C. In summary, the current study shows that a combination of early quantitative serum HBsAg and HBV DNA levels allows the best selection of patients with HBeAg-negative CHB who will not respond to a 48-week course of peginterferon alfa-2a therapy. The discontinuation of peginterferon therapy and a switch to an alternative treatment appear to be indicated in patients without a decline in HBsAg levels combined with a

decline in HBV DNA levels of less than 2 log copies/mL at week 12. In addition to the MCE公司 authors, the study group includes the following members: in Austria, P. Munda, T. M. Scherzer, and K. Staufer (Medical University of Vienna, Vienna) and W. Vogel and I. Graziadei (Innsbruck Medical University, Innsbruck); in Germany, G. Gerken (University Hospital Essen, Essen) and C. Niederau (St. Josef Hospital Oberhausen, Oberhausen); in Greece, G. Germanidis (Papageorgiou General Hospital, Thessaloniki), G. Hatzis (Laikon General Hospital, Athens), G. Kitis and P. Xiarchos (George Papanikolaou Hospital, Thessaloniki), M. Raptopoulou-Gigi, E. Gigi, and E. Sinakos (Aristotle University of Thessaloniki, Thessaloniki), and I. Vafiadis-Zouboulis, P. Nicolaou, and G. Paraskevi (University of Athens Medical School, Athens); in Italy, P. Grima (S. Caterina Novella Hospital, Galatina), G. Montalto (Universita di Palermo, Palermo), M. Russello (Azienda Ospedaliera Garibaldi–Nesima, Catania), G. Scifo (Presidio Ospedaliero Muscatello, Augusta), A. Spadaro (University Hospital Messina, Messina), and S. Tripi (Universita di Palermo, Palermo); in the Netherlands, M. F. C. Beersma, M. L. op den Brouw, S. D. Diepstraten, G. J. van Doornum, C. van der Ent, A. Heijens, A.

30-32 Furthermore, this HBV DNA threshold and the duration of follow-up correspond with the definition of response to peginterferon therapy according to the recent European guidelines and the pivotal studies on peginterferon in CHB, respectively.10, 20, 33 The large majority of our patients were of Caucasian

origin and were infected with HBV genotypes A and D. Responsiveness to interferon-based therapy appears to be lower in patients with genotype PD0325901 D versus patients with other genotypes, and this may explain the limited efficacy of peginterferon in our study population.9, 10, 26, 34 A recent retrospective analysis of 264 HBeAg-negative patients treated with peginterferon alfa-2a alone or in combination with lamivudine

reported that pretreatment HBsAg levels varied according to Ku-0059436 mouse the genotype. The highest concentrations were found in patients infected with genotypes A and D. Although serum HBsAg levels decreased during the treatment phase for all genotypes, the HBsAg decline was least pronounced in patients with genotype D.35 Therefore, our data on the decline in HBsAg levels need to be confirmed in patients with genotypes B and C. In summary, the current study shows that a combination of early quantitative serum HBsAg and HBV DNA levels allows the best selection of patients with HBeAg-negative CHB who will not respond to a 48-week course of peginterferon alfa-2a therapy. The discontinuation of peginterferon therapy and a switch to an alternative treatment appear to be indicated in patients without a decline in HBsAg levels combined with a

decline in HBV DNA levels of less than 2 log copies/mL at week 12. In addition to the MCE authors, the study group includes the following members: in Austria, P. Munda, T. M. Scherzer, and K. Staufer (Medical University of Vienna, Vienna) and W. Vogel and I. Graziadei (Innsbruck Medical University, Innsbruck); in Germany, G. Gerken (University Hospital Essen, Essen) and C. Niederau (St. Josef Hospital Oberhausen, Oberhausen); in Greece, G. Germanidis (Papageorgiou General Hospital, Thessaloniki), G. Hatzis (Laikon General Hospital, Athens), G. Kitis and P. Xiarchos (George Papanikolaou Hospital, Thessaloniki), M. Raptopoulou-Gigi, E. Gigi, and E. Sinakos (Aristotle University of Thessaloniki, Thessaloniki), and I. Vafiadis-Zouboulis, P. Nicolaou, and G. Paraskevi (University of Athens Medical School, Athens); in Italy, P. Grima (S. Caterina Novella Hospital, Galatina), G. Montalto (Universita di Palermo, Palermo), M. Russello (Azienda Ospedaliera Garibaldi–Nesima, Catania), G. Scifo (Presidio Ospedaliero Muscatello, Augusta), A. Spadaro (University Hospital Messina, Messina), and S. Tripi (Universita di Palermo, Palermo); in the Netherlands, M. F. C. Beersma, M. L. op den Brouw, S. D. Diepstraten, G. J. van Doornum, C. van der Ent, A. Heijens, A.

31)8 were synthesized in the

Medicinal Chemistry Laboratory of the Institute of Medicinal Biotechnology Chinese Academy of Medical Sciences, with a purity over 99.0%. The compound structure was confirmed with 1H-NMR and MS spectra. Interferon-α-2b (Intron A) was from Schering Plough (Brinny) (Kenilworth, NJ). BILN2061, a known NS3-4A protease inhibitor, was provided by Shanghai Lechen International Trading (Shanghai, China). Plasmid pcDNA3.1-Vif coding for HIV-1 full-length Vif was created by insertion of Vif (amplified ABT-263 chemical structure by polymerase chain reaction [PCR] from HIV-1 plasmid SVC21.BH10) into pcDNA3.1; the plasmids hA2, hA3B, hA3C, hA3F, and hA3G that express wildtype forms of hA2, hA3B, hA3C, hA3F, and hA3G, respectively, possess a fused HA tag at the C-terminus. The above-mentioned plasmids were gifts from Dr. Shan Cen at the Lady Davis Institute for Medical Research and McGill University AIDS Centre. The plasmid pFL-J6/JFH/JC1 containing the full-length chimeric

HCV cDNA was kindly provided by Vertex Pharmaceuticals (Boston, MA). Production of infectious HCV in hepatocytes was done as described.14 The plasmid pFL-J6/JFH/JC1 was restricted with XbaI and treated with Mung Bean nuclease (New England Biolabs) to generate the according HCV cDNA with T7 promotor. The cDNAs were purified and used as templates for RNA synthesis. HCV RNA was synthesized MCE公司 in vitro using a MEGAscript T7 kit (Ambion). The synthesized RNA was treated

with DNase I (New England Biolabs) and purified with Wizard Midostaurin clinical trial SV Gel and PCR Clean-Up System (Promega). The synthesized HCV RNA was used to transfect naïve Huh7.5 cells with the addition of Lipofectamine 2000 (Invitrogen). The culture medium was collected and cleaned with centrifugation at 3,000 rpm for 10 minutes. The supernatants were stored at −70°C as HCV viral stock and quantified with the Diagnostic Kit for Quantification of Hepatitis C Virus RNA (Shanghai Kehua Bio-Engineering). Huh7.5 cells 24 hours after HCV infection with viral stock (45 IU per cell) were transfected with different concentrations of APOBEC- or Vif-containing plasmids in the FuGENE HD Transfection Reagent (Roche), with pcDNA3.1 as plasmid control. Then, 72 hours later the culture medium was removed and total intracellular proteins were extracted using CytoBuster Protein Extraction Reagent (Novagen) with 1 mM protease inhibitor cocktail (Roche Applied Science). HCV Core, NS3, and hA3G protein (or APOBEC proteins with HA tag) was detected with western blot. A similar procedure was used for the experiment using GS4.3 cells, except the infection step. Huh7.5 cells were planted into the 6-well plate with 3 × 105 cells per well in the complete growth medium and infected with HCV viral stock (45 IU per cell).

2B), indicating that CD59 is related selleck compound library to the HCV particles. All fractions collected from the supernatant of uninfected Huh7.5.1 cells were

HCV core and RNA negative and CD59 negative (Fig. 2B). To further exclude the possibility of host cell protein contamination, a virus capture assay was utilized. In agreement with the previous report,5 HIV-1 particles were captured by anti-human CD59 pAbs, as HIV-1-specific qPCR qualified 167 copies of HIV-1 RNA from an input of 2,000 viral RNA copies in 100 μL of supernatant (8.4% capture rate) (Fig. 2C). Similarly, HCV particles were also captured by the pAbs, although only 26 copies of viral RNA were detected by the qPCR from an input of 2,000 HCV copies in 100 μL of supernatant (1.3% capture rate) (Fig. 2C). HCV capture efficiency was markedly enhanced when the purified viral particles were used, as 215 copies of viral RNA were detected learn more from an input of 2,000 HCV copies of the purified

virus fraction 3 resuspended in 100 μL of supernatant from uninfected Huh7.5.1 cells (10.8% capture rate) (Fig. 2D). Thus, anti-human CD59 Abs captured HCV, which directly shows the presence of CD59 on the external membrane of HCV particles. To further investigate whether primary HCV virions also incorporate CD59, we purified HCV particles from the plasma of five HCV-infected individuals by sucrose gradient ultracentrifugation as described above. The purified primary virions were subjected to western blot for measuring CD59. As shown in Fig. 3, CD59 was detected by western blot from virus particles purified from plasma samples of all five HCV-infected patients examined (Pt1 to Pt5; Table 1), but not from any of the three HCV-negative healthy donors (H1 to H3).

Importantly, CD59 levels correlated with plasma HCV viral loads (Fig. 3), suggesting MCE that the CD59 signal is derived from HCV particles rather than potential contamination of host proteins coprecipitated from plasma samples. To test whether CD59 incorporation protects HCV against ADCML, we used BRIC229 and rILYd4 to block CD59 and then analyzed HCV lysis in the presence or absence of anti-HCV E2 pAbs with or without competent complement. As shown in Fig. 4A, HCV core was markedly increased in both BRIC229 and rILYd4 treatments in a dose-dependent manner when compared with PBS or IgG control. The increase of HCV core was triggered by ADCML because the effects of BRIC229 and rILYd4 were completely abolished if heat-inactivated complement was used or anti-HCV E2 pAbs were replaced with anti-HIV-1 gp120/160 pAbs (Fig. 4A,B). Notably, moderate levels of HCV core were detected in PBS control groups in the presence (13.6 ± 1.9 ng/mL, n = 3) or absence (12.6 ± 2.6 ng/mL, n = 3) of complement activation when compared with the maximal lysis of Triton X-100 treatments in the presence (36.3 ± 2.9 ng/mL, n = 3) or absence of complement activation (35.7 ± 3.6 ng/mL, n = 3) (Fig.

Although AFS is known to result in bone erosion, invasive complications are rare. The clinical and pathologic information were reviewed. A literature review was

performed to clarify the clinical, radiologic, and pathologic features of AFS. The clinical and radiographic presentations were typical for AFS, including the relatively common complication of sinus wall erosion. Follow-up imaging demonstrated spread of fungal disease into the adjacent masticator space and intracranial spread by foramen ovale. This case illustrates the importance of identifying AFS and describing findings such as sinus erosion that may alter management. In this example, knowledge of the altered anatomy and potential learn more for mucosal injury may facilitate surgical planning and decrease the likelihood of future complications. The patient was a 14-year-old female who initially presented to her pediatrician with chronic sinus congestion, gray drainage, and facial swelling with asymmetry. These symptoms prompted a sinus CT scan and referral to an otolaryngologist. The CT scan (Fig 1) demonstrated findings compatible with allergic fungal sinusitis (AFS), including high attenuation secretions, marked Saracatinib sinus expansion, and multiple areas of bony thinning and focal dehiscence.[1] In particular, there was a large erosion involving the lateral wall of her right sphenoid sinus. Despite initial conservative management with nasal irrigation and steroids, the symptoms persisted,

and endoscopic sinus surgery was performed with bilateral ethmoidectomies, maxillary antrostomies, frontal sinus exploration, and sphenoid osteotomy. She was also treated at this time with antibiotics because of a positive pseudomonas culture. Although her initial postoperative course was uncomplicated, sinus drainage persisted and she developed jaw pain. A dental workup at this time was unremarkable. Her condition suddenly worsened a year later when she experienced two seizures and was taken to the emergency department for further evaluation. MR imaging

workup at this time revealed a peripherally enhancing mass with restricted diffusion extending from the infratemporal fossa into the middle cranial fossa (Fig 2). On the basis of these imaging findings, the differential considerations 上海皓元 included abscess or neoplasm, such as lymphoma or primary head and neck tumor. Features more typical for abscess in this case include the T2 hypointense rim, central pattern of diffusion restriction, and possible “daughter” or satellite lesions.[2, 3] CT scanning showed the infratemporal portion of the mass to be adjacent to the previously seen sphenoid sinus erosion (Fig 3), suggesting the erosion as a mechanism for extrasinus spread of disease. The patient underwent right temporal craniotomy and intracranial abscess drainage. Initial potassium hydroxide preparation demonstrated septate fungal hyphae, and aspergillus fumigatus was isolated from fungal cultures.

These steps are necessary since signature metabolites will HIF inhibitor not be detected by routine methods for bile acid measurement. With Setchell’s methodology

established, we were ready to screen infants with cholestasis. In 1988 male twins who presented with cholestasis and coagulopathy in the first days of life were referred to us for further evaluation. A similarly affected sibling had died at 4 months of age 3 years previously with what was called “idiopathic neonatal hepatitis / giant cell hepatitis.” Our initial evaluation of the twins strongly suggested a defect in bile acid biosynthesis. Setchell’s lab was able to document that their rate of primary bile acid synthesis was reduced, that cholic acid was absent from blood, and that gallbladder bile contained only trace amounts

of bile acids. Urine served as the main route of excretion, with the excreted compounds in the form of Δ4−3-oxo bile acids. This biochemical picture suggested a defect in bile acid synthesis—specifically, a lack of conversion of Δ4−3-oxo intermediates to 3α-hydroxy-5β products, a reaction catalyzed by cytosolic Δ4−3-oxosteroid 5β-reductase[66] (Fig. Cobimetinib research buy 5). The presumed pathophysiology of the hepatocellular and bile ductular injury was directly attributed to inadequate synthesis of primary bile acids (cholic) needed to generate bile acid-dependent bile flow, and accumulation of hepatotoxic Δ4−3-oxo bile acids. MCE公司 These precursors were shown to act as cholestatic agents by inhibiting canalicular adenosine triphosphate (ATP)-dependent bile acid transport, the rate-limiting step in the overall process of bile acid transport across the hepatocyte.[67] Of interest, electron microscopy of the twins liver biopsies revealed abnormal collapsed bile canaliculi, suggesting that maturation of the canalicular membrane and transport system for bile acid excretion requires a threshold concentration of primary bile acids in early

development.[68] This was consistent with studies of fetal rat liver, in which poorly formed bile canaliculi can be demonstrated by histology and immunocytochemistry.[69, 70] Bile canalicular morphologic maturation in the immediate postnatal period correlates with transition and acceleration of bile acid synthesis. This demonstrates the relationship between the pattern and pace of bile acid synthesis in fetal and neonatal rat liver and bile canalicular development. In the analogy to CAH syndromes, we chose to use cholic acid (3α,7α,12α-trihydroxy-5β-cholanoic acid) as replacement therapy to treat these twins with Δ4−3-oxosteroid 5β-reductase deficiency.

Unfortunately, little is known about its role in the process of tumor angiogenesis. In this study, we investigated the effects

and potential mechanisms of parthenolide INK 128 purchase on angiogenesis in human colorectal cancer (CRC). Methods: HUVEC, human umbilical vein endothelial cells, was treated with PT at different concentrations. The MTT assay and flow cytometry analysis using PI were used to analyze cell death. We determined the effect of PT on tube formation and migration in HUVEC cells. Then, protein level of the angiogenesis related factors such as VEGF, VEGFR-1 and VEGFR-2 were observed in HUVEC cells and human colorectal cancer cells (HT-29, SW620, HCT-116). HT-29 cells xenograft model in nude mice was also used to investigate the in vivo inhibitory effects on angiogenesis by PT. Results: Suppression of proliferation, migration, selleck chemicals llc and the tube formation capacity of HUVEC cells were observed after PT treatment. Angiogenesis related

proteins are also decreased by PT in HUVEC cells. Moreover, PT effectively inhibited proliferation of colorectal cancer cells and expression of angiogenesis related proteins in vitro. Intraperitoneal injection of PT showed significant inhibition of growth in the xenograft model via decreased production of VEGF. Conclusion: These results demonstrate that PT exhibits inhibitory effect on angiogenesis in human colorectal cancer in vitro and in vivo. Key Word(s): 1. MCE Angiogenesis; 2. Colorectal cancer; 3. Parthenolide; 4. Apoptosis; Presenting Author: DEQIANG HUANG Additional Authors: HUI LIN, SANSAN JIANG, NIANSHUAN NIANSHUAN, LINGYU LUO, NONGHUA NONGHUA Corresponding Author: NONGHUA NONGHUA Affiliations: The first affilated hospital of Nanchang University; The first affiliated hospital of Nachang University; The first affiliated hospital

of Nanchang University; The first affiliated hospital of Nanchang university Objective: Metformin, a derivative of biguanide, is a first-line therapy for type 2 diabetes mellitus, Previous studies have demonstrated the anti-cancer activity of metformin in various types of cancer cells, However, the manner in which metformin regulate migration or related epithelial-to-mesenchymal transitions (EMT) has yet to be elucidated. The aim of this study was to explore the effect of meformine on growth and migration using AGS gastric cancer cells. Methods: Cell viability was determined by the conventional MTT assay; Cell migration (wound healing) assay was conducted to determine the capacity of cell migration; The expression of EMT markers was analyzed by Western blotting. Results: We found that metformin reduced growth of AGS cells in a dose-dependent manner (Fig. 1). In addition, the drug significantly inhibited the migration of AGS cells (Fig. 2). Furthermore (Fig. 3), metformin strongly decreased vimentin (a mesenchymal marker) expression, while increasing E-cadherin (an epithelial marker) expression.