A polyglycolic acid mesh (PGA) served as a reference


A polyglycolic acid mesh (PGA) served as a reference

group. Controls were analyzed 48 h after seeding porcine chondrocytes via scanning electron microscopy (SEM), DNA, and glycosaminoglycan (GAG) quantifications. constructs were cultured Crenolanib solubility dmso for 21 days prior to confocal microscopy, SEM, histology, and quantitive analysis (weight, water, DNA, GAG and collagen II). Chondrocytes maintained their phenotypic appearance and a viability above 85% oil the chitosan scaffolds. Chondrocytes attach preferentially to PGA, resulting in a greater cellularity of these constructs. However, based oil the GAG/DNA and Collagen II/DNA ratios, matrix production per chondrocyte was improved ill chitosan Constructs, especially on smaller fibers. The differences between PGA and chitosan are more likely to result from the chemical composition rather than their structural characteristics. Although chitosan appears to promote selleck inhibitor matrix formation, further Studies should be aimed at improving its cell adhesion properties. (C) 2009 Wiley Periodicals, Inc. I Biomed Mater Res 93A: 46-55, 2010″
“Objective To compare experiences, attitudes, and beliefs of immigrant and nonimmigrant women presenting for abortion with regard to contraception,

and to identify difficulties involved in accessing contraception in Canada.\n\nDesign A survey of immigrant and nonimmigrant women asking about women’s experiences with and attitudes toward contraceptives and any barriers to contraceptive access they have encountered. Demographic data including ethnicity, country of origin, and length of residence in Canada

were collected.\n\nSetting Two urban abortion clinics.\n\nParticipants Women presenting for first-trimester abortion.\n\nMain outcome measures Type of contraception used when the unwanted pregnancy was conceived, attitudes to contraceptives, and barriers to access of contraceptives.\n\nResults A total of 999 women completed questionnaires during the study period (75.9% response rate); 466 of them (46.6%) were born in Canada. Immigrant women presenting for abortion were less likely to be using hormonal contraception when SNS-032 concentration they got pregnant (12.5% vs 23.5%, P<.001) and had more negative attitudes toward hormonal contraception (62.6% vs 51.6%, P<.003). They reported having more difficulties accessing contraception before the abortion (24.8% vs 15.3%, P<.001) than nonimmigrant women did. About half of all the women expressed fear about intrauterine device use. The longer immigrant women had lived in Canada, the more likely they were to have similar responses to those of Canadian-born women.\n\nConclusion The information provided by this study might be valuable for family doctors and other clinicians to improve contraceptive information resources for immigrants to address existing knowledge gaps and other culturally relevant concerns.

We investigated whether the R53H loss-of-function polymorphism of

We investigated whether the R53H loss-of-function polymorphism of the human tissue kallikrein gene affects renal potassium handling. In a crossover study, 30 R53R homozygous and 10 R53H heterozygous healthy males were randomly assigned to a low-sodium/high-potassium

or a high-sodium/low-potassium diet to modulate tissue kallikrein synthesis. On the seventh day of each diet, participants were studied before and during a 2-h infusion of furosemide to stimulate distal potassium Navitoclax Apoptosis inhibitor secretion. Urinary kallikrein activity was significantly lower in R53H than in R53R subjects on the low-sodium/high-potassium diet and was similarly reduced in both genotypes on high-sodium/low-potassium. Plasma potassium and renal potassium reabsorption were similar in both genotypes on an ad libitum sodium/potassium diet or after 7 days of a high-sodium/low-potassium diet. However, the median plasma potassium was significantly higher after 7 days of low-sodium/high-potassium diet in R53H than in R53R individuals. Urine potassium excretion and plasma aldosterone concentrations were similar. On the low-sodium/high-potassium diet, furosemide-induced decrease in plasma potassium was significantly larger in R53H than in R53R subjects. Thus, impaired tissue kallikrein

stimulation by a low-sodium/high-potassium diet in R53H subjects with partial tissue kallikrein deficiency highlights an inappropriate renal adaptation to potassium load, consistent with experimental data in mice.”
“Patterned films of poly(styrene-co-maleic GW786034 inhibitor anhydride) copolymers were deposited by dip-coating from acetone solutions. A qualitative study of the film morphologies shows LY3023414 order the formation of polymer spheres with smaller diameters at higher amounts of maleic anhydride (MA), and long-fibrous features at higher molecular weights. Upon heating, the films progressively re-assemble with short- and long-fibrous structures as a function of heating time and temperature. In parallel, the film morphologies are quantified by image processing and filtering

techniques. The differential scanning calorimetry confirms the higher glass transition temperatures with increasing amount of MA. The analysis with Raman spectroscopy shows interactions between the molecules in solution and effects of ring-opening (hydrolysis) and ring-closure (formation of MA) during drying of the films. The water contact angles on the patterned films are within the hydrophilic range. They mainly correlate with the amount of MA moieties calculated from spectroscopy, while the roughness parameters have a minor effect. The variations in film patterns illustrate the self-assemble ability of the copolymers and confirm a heterogeneous molecular structure, as previously assumed.”
“BackgroundPrediction of a woman’s risk of a spontaneous preterm delivery (PTD) is a core challenge and an unresolved problem in today’s obstetric practice. The objective of this study was to develop prediction models for spontaneous PTD ( smaller than 37 weeks).

“We aimed at validating the role of genetic variants ident

“We aimed at validating the role of genetic variants identified by a recent genome-wide association study (GWAS) as determinants of chronic oxaliplatin-induced peripheral neurotoxicity (OXAIPN). Eight polymorphisms (rs10486003, rs2338, rs843748, 5-Fluoracil cost rs797519, rs4936453, rs12023000, rs17140129, and rs6924717) were genotyped in a total of 150 colorectal cancer patients of Caucasian origin receiving oxaliplatin-based chemotherapy. The severity grade of chronic OXAIPN was assessed by NCI-CTC criteria and the clinical version of the Total Neuropathy Score((c)) (TNSc (c)). None of the polymorphisms investigated was found associated with grade 2 chronic OXAIPN (NCI-CTC criteria), while a nominal association

emerged for ACYP2 rs843748 when using the TNSc (c) scale (dominant model: odds ratio [OR]: 0.27, 95% confidence interval [CI]: 0.10-0.75, P=0.008). In the combined analysis of this results with data of the two previously published studies which assessed Adriamycin chronic OXAIPN by NCI-CTC criteria, evidence suggestive of association with chronic OXAIPN (NCI-CTC criteria) was found for ACYP2 rs843748 (dominant model: OR: 2.40, 95%CI: 1.40-5.24, P=0.027), which, however, did not remain significant after correction for multiple testing (threshold P-value smaller than 0.00625). These findings suggest a minor role of the single nucleotide polymorphisms

(SNPs) investigated as genetic determinants of chronic OXAIPN. These results also highlight the importance of replication studies with meta-analysis for validation of GWAS findings.”
“Genetic variants of cytochrome P450 2C9 (CYP2C9) and vitamin K epoxide reductase (VKORC1) are known to influence warfarin dose, but the effect of other genes has not been fully elucidated. We genotyped 183 polymorphisms in 29 candidate genes in 1496 Swedish patients starting warfarin treatment, and tested for association with response. CYP2C9*2 and *3 explained 12% (P = 6.63 x 10(-34))

of the variation in warfarin dose, while a single VKORC1 SNP explained 30% (P = 9.82 x 10(-100)). No SNP outside the CYP2C gene cluster and VKORC1 regions was significantly associated with dose after correction for multiple Panobinostat cell line testing. During initiation of therapy, homozygosity for CYP2C9 and VKORC1 variant alleles increased the risk of over-anticoagulation, hazard ratios 21.84 (95% CI 9.46; 50.42) and 4.56 (95% CI 2.85; 7.30), respectively. One of 8 patients with CYP2C9*3/*3 (12.5%) experienced severe bleeding during the first month compared with 0.27% of other patients (P = .066). A multiple regression model using the predictors CYP2C9, VKORC1, age, sex, and drug interactions explained 59% of the variance in warfarin dose, and 53% in an independent sample of 181 Swedish individuals. In conclusion, CYP2C9 and VKORC1 significantly influenced warfarin dose and predicted individuals predisposed to unstable anticoagulation.

“Background: Infection with high-risk type human papilloma

“Background: Infection with high-risk type human papilloma viruses (HPVs) is associated with cervical carcinomas and with a subset of head and neck squamous cell carcinomas. Viral E6 and E7 oncogenes cooperate to achieve cell immortalization by a mechanism that is not yet fully understood. Here, human keratinocytes were immortalized by long-term expression of HPV type 16 E6 or E7 oncoproteins, or both. Proteomic profiling TGF-beta pathway was used to compare expression levels for 741 discrete protein features.\n\nResults: Six replicate measurements were performed for each group using two-dimensional difference gel electrophoresis (2D-DIGE). The median within-group coefficient

of variation was 19-21%. Significance of between-group differences was tested based on Significance Analysis of Microarray and fold change. Expression of 170 (23%) of the protein features changed significantly in immortalized cells compared to primary keratinocytes. Most of these changes were qualitatively similar in cells immortalized by E6, E7, or E6/7 expression, indicating convergence on a common phenotype, but fifteen proteins (similar to 2%) were outliers in this regulatory pattern. Ten demonstrated opposite regulation in E6- and E7-expressing cells, including the

cell cycle regulator p16(INK4a); the carbohydrate binding protein Galectin-7; two differentially migrating forms of the intermediate filament protein Cytokeratin-7; Citarinostat cost HSPAIA (Hsp70-1); and five unidentified proteins. Five others had a pattern of expression that suggested cooperativity between the co-expressed oncoproteins. Two of these were identified as forms of the small heat shock protein HSPB1 (Hsp27).\n\nConclusion: This large-scale analysis provides a framework for understanding the cooperation between E6 and E7 oncoproteins in HPV-driven carcinogenesis.”
“Specific protein interactions are responsible for most biological functions. Distinguishing selleck screening library Functionally Linked Interfaces of Proteins (FLIPs), from Functionally uncorrelated

Contacts (FunCs), is therefore important to characterizing these interactions. To achieve this goal, we have created a database of protein structures called FLIPdb, containing proteins belonging to various functional sub-categories. Here, we use geometric features coupled with Kortemme and Baker’s computational alanine scanning method to calculate the energetic sensitivity of each amino acid at the interface to substitution, identify hotspots, and identify other factors that may contribute towards an interface being FLIP or FunC. Using Principal Component Analysis and K-means clustering on a training set of 160 interfaces, we could distinguish FLIPs from FunCs with an accuracy of 76%. When these methods were applied to two test sets of 18 and 170 interfaces, we achieved similar accuracies of 78% and 80%.

Finally, expression of TLR9 was studied in clinical breast cancer

Finally, expression of TLR9 was studied in clinical breast cancer samples and normal breast epithelium with immunohistochemistry. TLR9 staining localized in epithelial cells Duvelisib in both cancer and normal samples. The mean TLR9 staining intensity was significantly increased in the breast cancer cells compared with normal breast epithelial cells. In conclusion, our results suggest that TLR9 expression is increased in breast cancer and CpG oligonucleotide-induced cellular

invasion is mediated via TLR9 and TRAF6, independent of MyD88. Further, our findings suggest that the structure and/or stability of DNA may influence the induction of TLR9-mediated invasion in breast cancer. (Mol Cancer Res 2008;6(10):1534-43)”
“There is an urgent requirement for unraveling the pathway for biosynthesis of the polysaccharide YCP from the marine fungus Phoma herbarum YS4108 in order to exploit its potential as an anti-tumor agent. Here we present cloning and characterization LY2835219 mouse of UDP-glucose 6-dehydrogenase (UDP-GlcDHase), a key enzyme for the biosynthesis

of this glycan. A full-length cDNA encoding UDP-GlcDHase was obtained by PCR using degenerate primers and the RACE strategy. The cDNA was 1846 bp in length with an open reading frame of 1560 bp encoding a protein of 520 amino acids. The deduced amino acid sequence showed about 50% overall identity to its homologs and a high degree of conservation in the nucleotide binding and catalytic domains. The cDNA was cloned in the Pichia pastoris GS115 on the plasmid vector, pPIC3.5k, to allow inducible expression of the protein with an N-terminal histidine-tag. Recombinant UDP-GlcDHase was affinity purified from crude, cytosolic extracts of the host cells, and characterized in terms of the its substrate affinity and the optimum temperature and pH for its activity. The biochemical properties of the purified recombinant Erastin enzyme were comparable with those of its homologs. The present investigation provides a promising start

for manipulating YCP biosynthesis in P. herbarum. (C) 2011 Elsevier Ltd. All rights reserved.”
“Objectives: To evaluate whether age and gender differences are predictive factors for inferior alveolar nerve position with respect to mandibular first molar roots.\n\nStudy Design: Cone-beam computed tomography scans [0.2-mm(3) voxel size; n = 200 (100 males, 100 females)] of patients aged 15-65 years showing mandibular first and second molars were included in this study. Patients with pathoses that might affect inferior alveolar nerve position, including second molar and/or first premolar extraction, were excluded. Fourteen measurements (mm) were taken from the inferior alveolar nerve to the mesial and distal root apices. Subjects were grouped by age and gender. Data were analysed using two-way analyses of variance with post hoc Bonferroni corrections.

Methods We evaluated the utility of the PHI measure using 409 LLI

Methods We evaluated the utility of the PHI measure using 409 LLINs collected over three years in Nampula Province, Mozambique following a mass distribution campaign in 2008. For each LLIN the diameter and distance from the bottom of the net were recorded for every hole. Holes were classified into four size categories and a PHI was calculated following WHOPES guidelines. We investigate how the size, shape, and location of

holes influence the PHI. The areas of the WHOPES defined categories were compared to circular and elliptical areas based on approximate shape and actual measured click here axes of each hole and the PHI was compared to cumulative damaged surface area of the LLIN. Results The damaged area of small, medium, large, and extra-large holes was overestimated using the WHOPES categories compared to elliptical areas using the actual measured axes. Similar results were found when comparing to circular areas except for extra-large holes which were underestimated. (Wilcoxon signed rank test of differences p smaller than 0.0001

for all sizes). Approximating holes as circular overestimated hole surface area by 1.5 to 2 times or more. There was a significant difference in the mean number of holes smaller than GW3965 0.5 cm by brand and there were more holes of all sizes on the bottom of nets than the top. For a range

of hypothetical PHI thresholds CT99021 used to designate a “failed LLIN”, roughly 75 to 80% of failed LLINs were detected by considering large and extra-large holes alone, but sensitivity varied by brand. Conclusions Future studies may refine the PHI to better approximate overall damaged surface area. Furthermore, research is needed to identify whether or not appropriate PHI thresholds can be used to deem a net no longer protective. Once a cutoff is selected, simpler methods of determining the effective lifespan of LLINs can help guide replacement strategies for malaria control programs.”
“Cyclin-dependent kinase 1 (Cdk1) is required for initiation and maintenance of polarized cell growth in budding yeast. Cdk1 activates Rho-family GTPases, which polarize the actin cytoskeleton for delivery of membrane to growth sites via the secretory pathway. Here we investigate whether Cdk1 plays additional roles in the initiation and maintenance of polarized cell growth. We find that inhibition of Cdk1 causes a cell surface growth defect that is as severe as that caused by actin depolymerization. However, unlike actin depolymerization, Cdk1 inhibition does not result in a massive accumulation of intracellular secretory vesicles or their cargoes.

Here we exploited the behavioral differences between good and poo

Here we exploited the behavioral differences between good and poor avoiders to elucidate

the AA neurocircuit. Rats received Sidman AA training and expression of the activity-dependent immediate-early gene c-fos was measured after a shock-free AA test. Six brain regions with known or putative roles in AA were evaluated: amygdala, periaqueductal gray, nucleus accumbens, dorsal striatum, prefrontal cortex (PFC), and hippocampus. Good avoiders showed little Pavlovian freezing and high AA rates at test, the opposite of poor avoiders. Although c-Fos activation was observed throughout the brain, differential activation was found only in subregions of amygdala and PFC. Interestingly, selleck c-Fos correlated with avoidance and freezing in only five of 20 distinct areas evaluated: lateral amygdala, central amygdala, medial amygdala, basal amygdala, and infralimbic PFC. Thus, activity in specific amygdala-PFC circuits likely mediates the competition between instrumental actions and Pavlovian reactions after AA training. Individual differences in AA behavior, long considered a nuisance by researchers, may be the key to elucidating the AA Nepicastat neurocircuit and understanding pathological response profiles.”
“Background Acute posttraumatic tracheobronchial lesions are rare events associated with significant

morbidity and mortality. They are caused by blunt and penetrating trauma, or they are iatrogenic, appearing after intubation or tracheotomy. Although surgery has traditionally been considered the treatment of choice for these injuries, recent reports show that conservative treatment can be effective in selected patients. The aim of this Kinase Inhibitor Library study was to evaluate the role of surgical and conservative management of these lesions, differentiated on the basis of clinical and endoscopic criteria.\n\nMethods From January 1993 to October 2010, a total of 50 patients with acute posttraumatic tracheobronchial lesions were referred for treatment to our department. In all, 36 patients had iatrogenic injuries of the airway, and 14 had

lesions resulting from blunt or penetrating trauma.\n\nResults Of the 30 patients who underwent surgery, the lesion was repaired with interrupted absorbable sutures in 29; the remaining patient, with an associated tracheoesophageal fistula, underwent single-stage tracheal resection and reconstruction and closure of the fistula. In all, 20 patients were treated conservatively: clinical observation in 5 patients, airway decompression with a mini-tracheotomy cannula in 4 spontaneously breathing patients, and tracheotomy with the cuff positioned distal to the lesion in 11 mechanically ventilated patients. One surgical and one conservatively-managed patient died after treatment (4% overall mortality). Complete recovery and healing were achieved in all the remaining patients.

All patients underwent optical coherence tomography, best-correct

All patients underwent optical coherence tomography, best-corrected visual acuity (BCVA) measurement, and dilated fundus examination with indentation, pre- and postoperatively.\n\nResults: The mean (+/- standard deviation) follow-up time was 13 +/- 3 months (range 9-18). Postoperatively, all eyes demonstrated an attached retina, whereas MH closure was achieved in only 1 eye, and in a second

eye after additional injection of gas and further posturing. The BCVA improved from 2.2 +/- 0.4 logMAR (logarithm of the minimum angle of resolution) at baseline to 2.0 +/- 0.5 logMAR at the end of follow-up (p = .05).\n\nConclusion: The failure in MH closure in most of our cases strengthens the learn more view that short-term tamponade with SF(6) may not suffice for achieving MH closure, and either prolonged tamponade (with C(3)F(8) or silicone oil) or additional photocoagulation may be a better option for eyes with see more MHRDs. In addition, it is possible that intravitreal injection of gas might be an option for the treatment of persistent MHs after vitrectomy for MHRD, especially when the MH is small. Further studies are required to evaluate the above findings, although the implementation

of large series studies remains a challenge because of the rarity of cases with MHRDs.”
“We have defined proximal lower limb ischaemia as a decrease in Exercise-transcutaneous oxygen pressure (TcPO(2)) lower than minus 15 mmHg at the buttock level in patients with peripheral artery occlusive disease. The purpose of this study was to objectively evaluate the benefits of direct versus indirect revascularisation of internal iliac arteries (IIAs) for prevention of buttock claudication BIBF1120 in this population.\n\nWe retrospectively reviewed the charts of proximal ischaemia patients who underwent revascularisation and both preoperative and postoperative stress TcPO(2) testing. Revascularisation procedures were classified as either direct revascularisation, including percutaneous transluminal angioplasty and internal

iliac artery bypass, resulting in a direct inflow in a patent IIA (group 1) or indirect revascularisation, including aortobifemoral bypass and recanalisation of the femoral junction on the ischaemic side, resulting in indirect inflow from collateral arteries in the hypogastric territory (group 2). Patency was checked 3 months after revascularisation in all cases.\n\nTreadmill exercise stress tests were performed before and after revascularisation using the same protocol designed to assess pain, determine maximum walking distance (MWD) and measure TcPO(2) during exercise. In addition, ankle brachial indices (ABIs) were calculated.\n\nBetween May 2001 and March 2008, a total of 93 patients with objectively documented proximal ischaemia underwent 145 proximal revascularisation procedures using conventional open techniques in 109 cases and endovascular techniques in 36.

We demonstrated earlier that depletion of mitochondrial DNA (mtDN

We demonstrated earlier that depletion of mitochondrial DNA (mtDNA) induces prostate cancer progression. Here, using normal prostate epithelial PNT1A cells we demonstrate that mtDNA depletion prevents detachment-induced

apoptosis (anoikis) and promotes migratory capabilities onto basement membrane proteins through upregulation of p85 and p110 phosphatidylinositol 3-kinase (PI3K) subunits, which results in Akt2 activation and phosphorylation of downstream substrates GSK3 beta, c-Myc, MMP-9, Mdm2, and p53. Pharmacological or genetic PI3K inhibition, siRNA-mediated Akt2 depletion, as well as mtDNA reconstitution were sufficient to restore sensitivity to anoikis and curtail cell migration. Moreover, Akt2 activation induced glucose transporter 1 (GLUT1) expression,

Flavopiridol glucose uptake, and lactate production, common phenotypic changes seen in neoplastic cells. In keeping with these findings, several prostate carcinoma cell lines displayed reduced mtDNA content and increased PI3K/Akt2 levels when compared to normal PNT1A cells, and Akt2 downregulation prevented their survival, migration and glycolytic metabolism. On a tissue microarray, we also found a statistically significant decrease selleckchem in mtDNA-encoded cytochrome oxidase I in prostate carcinomas. Taken together, these results provide novel mechanistic evidence supporting the notion that mtDNA mutations may confer survival and migratory advantage to prostate cancer cells through Akt2 signaling.”
“There is increasing evidence linking the incidence of certain cancers to low serum Vitamin D levels. The

active metabolite of Vitamin D, calcitriol (1, 25-Dihydroxyvitamin D-3, 1,25(OH)(2)D-3) apart from a crucial role in maintaining mineral homeostasis and skeletal functions, has antiproliferative, apoptosis and differentiation inducing as well as immunomodulatory effects in this website cancer. In studying the role of 1,25(OH)(2)D-3 in cancer, it is imperative to examine the potential pathways that control local tissue levels of 1,25(OH)(2)D-3. The enzyme CYP24A1 or 24-hydroxylase converts 1,25(OH)(2)D-3 to inactive calcitroic acid. Extra-renal production of this enzyme is observed and has been increasingly recognized as present in cancer cells. This enzyme is rate limiting for the amount of local 1,25(OH)(2)D-3 in cancer tissues and elevated expression is associated with an adverse prognosis. The gene that encodes CYP24A1 has been reported as an oncogene and may contribute to tumor aggressiveness by abrogating local anti-cancer effects of 1,25(OH)(2)D-3. It is imperative to study the regulation of CYP24A1 in cancer and especially the local metabolism of 1,25(OH)(2)D-3 in cancer cells. CYP24A1 may be a predictive marker of 1,25(OH)(2)D-3 efficacy in patients with cancer as an adjunctive therapy.

Conclusions: Chemotherapy with rapamycin and etoposide combin

\n\nConclusions: Chemotherapy with rapamycin and etoposide combined is worth exploring as a treatment modality for women with epithelial ovarian cancer. Clin Cancer Res; 17(14); 4742-50. (C)2011 AACR.”
“Objective. To examine the biocompatibility of a novel nanohydroxyapatite/poly[lactic-co-glycolic acid] (nHA/PLGA) composite and evaluate its feasibility as a scaffold for cartilage tissue engineering. Methods. Chondrocytes of fetal rabbit were cultured with nHA/PLGA scaffold in vitro and the cell viability was assessed by MTT assay first. Cells adhering to nHA/PLGA scaffold see more were then observed by inverted

microscope and scanning electron microscope (SEM). The cell cycle profile was analyzed by flow cytometry. Results. The viability of the chondrocytes on the scaffold was not affected by nHA/PLGA comparing with the control group as it was shown by MTT assay. Cells on the surface and in the pores of the scaffold increased in a time-dependent manner. Results

obtained from flow cytometry showed that there was no significant difference in cell cycle profiles between the coculture group and control (P > 0.05). Conclusion. The porous nHA/PLGA composite scaffold is a biocompatible and good kind of scaffold for cartilage tissue engineering.”
“Background\n\nMultiple sclerosis (MS) is an immune-mediated disease of the central nervous system and a leading cause of disability in young and middle-aged adults. Mycophenolate mofetil (MMF) is an immunosuppressive agent that has been Sapanisertib purchase used for the prevention of allograft rejection after renal, cardiac, or liver

transplant and in patients with signaling pathway autoimmune diseases such as active relapsing-remitting (RRMS) and progressive MS.\n\nObjectives\n\nTo assess the efficacy and safety of MMF for preventing disease activity in patients with RRMS.\n\nSearch methods\n\nWe searched the Cochrane Multiple Sclerosis and Rare Diseases of the Central Nervous System Group Specialised Register (January 14, 2013). We searched three Chinese databases (January 2013) and checked reference lists of identified trials. We contacted authors and pharmaceutical companies to ask for additional information. We applied no language restrictions.\n\nSelection criteria\n\nWe included randomized controlled trials with a follow-up of at least 12 months that compared MMF as monotherapy or in combination with other treatments versus placebo, another drug, or the same cointervention as the treated group.\n\nData collection and analysis\n\nTwo review authors independently selected the trials for inclusion, assessed trial quality, and extracted data.\n\nMain results\n\nOne included study involving 26 participants with new-onset RRMS investigated the efficacy and safety of MMF (13 participants) versus placebo in interferon beta-1a-treated participants.