The efficacy and safety results after 24 months of treatment are reported here. Materials and methods Study design This randomized, double-blind, active-controlled, parallel-group study was conducted at 43 study centers in North America, South America, and the European Union. The first subject was screened in November 2007, and the last subject observation took place in April 2010. The study was performed in accordance with good clinical practice and the ethical principles that have their origin in the Declaration of Helsinki. The protocol was approved by the appropriate institutional review boards or ethics committees and the subjects gave written, Selleck ACY-1215 informed consent

to participate. The Identifier number for this study at Clinicaltrials.gov

was NCT00541658. Subjects This has been described in detail previously [1]. Postmenopausal women were eligible to participate in the study if they were at least 50 years of age, ambulatory, had osteoporosis defined as a BMD T-score in the lumbar spine or total hip of −2.5 or lower or a T-score of −2.0 or lower with at least one prevalent vertebral fracture (T4 to L4), and were in generally good health without contraindications to risedronate therapy or other reasons to not be in the clinical study. Those selleck chemicals llc subjects with baseline serum 25-hydroxyvitamin D levels <12 ng/ml were not eligible to participate in the study. Treatments Subjects were randomly assigned to one of three treatment groups: risedronate 5 mg IR daily or risedronate 35 mg DR once weekly before or immediately following breakfast. The minimization method of Pocock and Simon was used for randomization [8]. Eligible subjects who gave consent were stratified across study centers by anticoagulant use (since fecal occult blood testing was performed during the first 12 months of the study) and then randomly assigned within each study center in a 1:1:1 ratio to the three treatment groups. All subjects took nine study tablets each week: an IR tablet

or placebo before Lumacaftor breakfast daily; a 35-mg DR BMN 673 tablet or placebo before breakfast once weekly (DR BB); and another 35-mg DR tablet or placebo following breakfast once weekly (DR FB). All placebo tablets were identical in appearance to their corresponding active tablets (i.e., 5 mg IR or 35 mg DR) and supplied in identical blister cards. The 5-mg IR tablets and the 35-mg DR tablets assigned for before-breakfast intake were taken on an empty stomach in the morning at least 30 min before the first food or drink of the day; the 35-mg DR tablets assigned for following-breakfast intake were taken immediately after breakfast. All tablets were taken with at least 4 ounces of plain water, and subjects were instructed to remain in an upright position for at least 30 min after dosing. Compliance was assessed by tablet counts.

CrossRef Declaration of Competing interests The authors declare

that they have no competing interests. Authors’ contributions EEN was responsible for developing the concept and design of the study, data collection, statistical analysis and manuscript C188-9 manufacturer preparation. MJS, MLC, VAP and LKA contributed in the design of the study, data collection, and manuscript preparation. JB contributed with data analysis, statistical analysis, and manuscript preparation. All authors have read and approved the final draft of this manuscript.”
“Background Unaccustomed exercise, particularly eccentric exercise in which the muscle lengthens, is the most common method used to elicit muscle damage. Damaged muscle fibers initiate a cascade of reactions that result in a prolonged and complex interaction between Belinostat in vivo protein synthesis and degradation [1]. However, while protein turnover is elevated substantially, degradation usually exceeds synthesis, and thus, protein breakdown results, leading to muscle degeneration and atrophy [2]. These changes in muscle protein ultrastructure normally result in physiological symptoms such as reductions in muscle strength,

increased muscle soreness and impaired muscle function [3, 4]. Stimulating protein synthesis and minimizing protein breakdown (proteolysis) are the two cellular processes www.selleckchem.com/products/semaxanib-su5416.html that are essential for muscle recovery after damage [5]. While protein breakdown may be an important process involved in the adaptive response during recovery

[6], increasing protein synthetic rates within the muscle during the recovery period is vital for muscle regeneration and hypertrophy. Therefore, strategies that can promote a positive net muscle protein balance during the days following muscle injury are likely to increase the rate of protein synthesis, satellite cell proliferation, but more importantly, enhance the regenerative processes that would benefit athletes Prostatic acid phosphatase and others that perform strenuous/unaccustomed physical activity. Dietary proteins have an important role in regulating protein metabolism in skeletal muscle [7–9]. Whey protein isolate supplementation has been used effectively to increase muscle size and strength after resistance training [10], with some of these improvements thought to come from improved recovery from the exercise sessions. Compared to regular protein supplements, whey isolate is more effective at increasing blood amino acids and protein synthesis due to its different absorption kinetics and amino acid profile [11]. The high availability of amino acids in whey protein isolate, especially branched chain amino acids (BCAA), is important for protein synthesis in the hours immediately after ingestion. White et al. [12], examined the ingestion of a whey protein after an exercise bout which consisted of 50 maximal isokinetic eccentric quadricep contractions.

: FGFR1 emerges as a potential therapeutic target for lobular breast carcinomas. AZD2281 datasheet Clin Cancer Res 2006, 12:6652–6662.PubMedCrossRef 8. Ayers M, Fargnoli J, Lewin A, Wu Q, Platero JS: Discovery and validation

of biomarkers that respond to treatment with brivanib alaninate, a small-molecule VEGFR-2/FGFR-1 antagonist. Cancer Res 2007, 67:6899–906.PubMedCrossRef 9. Andre F, Bachelot TD, Campone M, Dalenc F, Perez-Garcia JM, Hurvitz SA, Turner NC, Rugo HS, Shi MM, Zhang Y, Kay A, Yovine AJ, Baselga J: A multicenter, open-label phase II trial of dovitinib, an FGFR1 inhibitor, in FGFR1 amplified and non-amplified metastatic breast cancer. J Clin Oncol 2011, 508:Suppl 508. 10. Koziczak M, Holbro T, Hynes NE: Blocking of FGFR signaling inhibits buy Adriamycin breast cancer cell proliferation through downregulation of D-type AZD3965 clinical trial cyclins. Oncogene 2004, 23:3501–3508.PubMedCrossRef 11. Brunelli M, Manfrin E, Martignoni G, Bersani S, Remo A, Reghellin D, Chilosi M, Bonetti F: HER-2/neu assessment in breast cancer using the original FDA and new ASCO/CAP guideline recommendations:

impact on selecting patients for herceptin therapy. Am J Clin Pathol 2008, 129:907–911.PubMedCrossRef 12. Perez EA, Spano JP: Current and emerging targeted therapies for metastatic breast cancer. Cancer 2012, 118:3014–25.PubMedCrossRef 13. Baselga J: Novel agents in the era of targeted therapy: what have we learned and how has our practice

changed? Ann Oncol 2008,19(Suppl 7):vii281-vii288.PubMedCrossRef 14. Massabeau C, Sigal-Zafrani B, Belin L, Savignoni A, Richardson M, Kirova YM, Cohen-Jonathan-Moyal E, Mégnin-Chanet F, Hall J, Fourquet A: The fibroblast growth factor receptor 1 (FGFR1), a marker of response to chemoradiotherapy in breast cancer? Breast Cancer Res Treat 2012, 134:259–266.PubMedCrossRef Guanylate cyclase 2C 15. Turner N, Pearson A, Sharpe R, Lambros M, Geyer F, Lopez-Garcia MA, Natrajan R, Marchio C, Iorns E, Mackay A, et al.: FGFR1 amplification drives endocrine therapy resistance and is a therapeutic target in breast cancer. Cancer Res 2010, 70:2085–2094.PubMedCrossRef 16. Dutt A, Ramos AH, Hammerman PS, Mermel C, Cho J, Sharifnia T, Chande A, Tanaka KE, Stransky N, Greulich H, et al.: Inhibitor-sensitive FGFR1 amplification in human non-small cell lung cancer. PLoS One 2011, 6:e20351.PubMedCrossRef 17. Gerlinger M, Rowan AJ, Horswell S, Larkin J, Endesfelder D, Gronroos E, Martinez P, Matthews N, Stewart A, Tarpey P, et al.: Intratumor heterogeneity and branched evolution revealed by multiregion sequencing. N Engl J Med 2012, 366:883–892.PubMedCrossRef 18. Courjal F, Cuny M, Simony-Lafontaine J, Louason G, Speiser P, Zeillinger R, Rodriguez C, Theillet C: Mapping of DNA amplifications at 15 chromosomal localizations in 1875 breast tumors: definition of phenotypic groups. Cancer Res 1997, 57:4360–4367.PubMed 19.

Micropor Mater 1997, 9:95–105.CrossRef 26. Ng EP, Nur H, Muhid MNM, Hamdan H: Sulphated AlMCM-41: mesoporous solid brønsted acid catalyst for dibenzoylation of biphenyl. Catal Today 2006, 114:257–262.CrossRef 27. Jones MD, Duer MJ: 29 Si cross polarisation magic angle spinning spectroscopic studies on MCM-41 supported with metal carbonyl clusters. Inorg Chim Acta 2003, 354:75–78.CrossRef 28. Kleitz F, Schmidt

W, Schüth F: Calcination behavior of different surfactant-templated mesostructured silica materials. Micropor Mesopor Mater 2003, 65:1–29.CrossRef NVP-BGJ398 purchase 29. Selvaraj M, Pandurangan A, Seshadri KS, Sinha PK, Lal KB: Synthesis, characterization and catalytic application of MCM-41mesoporous molecular sieves containing Zn and Al. Appl

Catal A: Gen 2003, 242:347–364.CrossRef 30. Kruk M, Jaroniec M, Sayari A: Adsorption study of surface and structural properties of MCM-41 materials of different pore sizes. J Phys Chem B 1997, 101:583–589.CrossRef ACY-1215 purchase Competing interests The authors declare that they have no competing interests. Authors’ contributions JYG carried out the main experimental work. EPN supervised the research activity and organized the manuscript. JYG and RRM did the chemical characterization. RRM, TCL, and EPN participated in the discussion of results and helped make critical comments in the initial draft of the manuscript. All authors read and approved the final manuscript.”
“Background Photonic-phononic crystals, also referred to as phoxonic crystals [1–4], are of great interest as their dual photonic and phononic bandgaps allow the simultaneous control of photon and phonon propagation in these crystals. Another class of metamaterials selleck compound possessing dual-excitation bandgaps is magnonic-phononic or magphonic crystals [5–7]. Although less well known than phoxonic materials, they too have promising application potential because of the possibility

of the simultaneous control and manipulation of magnon and phonon propagation in them. Hence, they are potentially more useful technologically than either solely magnonic or phononic crystals which depend on a single type of excitation, namely magnons or phonons, as the respective information carrier. Magphonic crystals were theoretically studied by Nikitov et al. in 2008 [5]. Recently, Zhang et al. experimentally studied SPTLC1 these materials in the form of a two-dimensional (2D) chessboard-patterned array of cobalt and Ni80Fe20 (Permalloy, Py) dots [6], and one-dimensional (1D) periodic arrays of alternating Fe (or Ni) and Py nanostripes on SiO2/Si substrates (henceforth referred to as Py/Fe(Ni)) [7]. As the materials of the elements of these bicomponent arrays are both metals, namely either Py/Co, Py/Fe, or Py/Ni, the elastic and density contrasts between adjacent elements are rather low. In general, the phononic bandgap width increases with elastic and density contrasts [8, 9]. Indeed the phonon bandgaps of the 1D and 2D structures measured by Zhang et al.

The use of a “”control diet”" is fundamentally important to researchers. Two types of “”control diets”" are frequently used in physiological studies: a commercial rodent diet (Purina®) and a diet proposed by the American Institute of Nutrition in 1993 (AIN-93) [12]. However, these two diets have different caloric contents Entinostat solubility dmso (Purina®: 3028.0 Kcal/kg and American Institute of Nutrition diet (AIN-93 M): 3802.7 Kcal/kg) that are not usually considered. Moreover, it is important to determine the possible effects of the feeding protocol and the different diets fed to rodents that are

used in exercise physiology studies. The lactate minimum test has been used in exercise physiology studies of both humans [13–16] and rodents [17–19] because it enables PFT�� manufacturer researchers to determine aerobic and anaerobic capabilities in a single test [20, 21]. However, the possible effects of administering diets with different caloric values and feed restriction on the parameters provided by the lactate minimum test are not well understood in the literature. Therefore, the

purpose of this study was to evaluate the effects of dietary restriction (60% of ad libitum intake) of two control diets (commercial Purina® and American Institute of Nutrition diet (AIN-93 M)) on the aerobic and anaerobic capacity of Wistar rats, as determined by the lactate minimum test. Methods Animals and animal care The duration of study was one month and we used 40 Wistar rats that were from 90 days old at the beginning of the find more experiment and had body weights of 406.9 ± 39.44 g. The animals were housed in polyethylene cages measuring 37 × 31 × 16 cm (five rats per cage) at room temperature (25°C) with a 12-hour light/dark photoperiod. All procedures involving animals were submitted to and approved by the Ethics Committee on Animal Use in Research of the Biosciences Institute of UNESP, Rio Claro Campus (protocol number: 2011/6274). The animals were divided into four groups Celecoxib with 10 animals per group, depending on the diet and mode of administration. Two groups had access to commercial feed (Purina®): one ad libitum

(ALP) and the other restricted (RAP). The two other groups had access to the diet proposed by the American Institute of Nutrition in 1993 (AIN-93 M): one ad libitum (ALD) and the other restricted (RAD). Feed intake for the animals in the ad libitum groups was recorded daily. Thus, for the animals on feed restriction, feed was offered in an amount corresponding to 60% of the average amount consumed by the ad libitum groups the previous day. This protocol was selected to allow for dietary restriction without causing malnutrition [4]. All groups had free access to water. Diet compositions Commercial Purina ® Diet (Paulínia/SP, Brazil) This diet was composed of 43.7% carbohydrates, 23% protein, and 4% fat at 3,028 kcal/g.

These results are also supported by the cell cycle analysis which showed very weak

effects on the stromal cells, only at 72 hrs at the highest concentration (Figure  6E-F). Figure 6 Effects of purified selleck chemicals llc recombinant protein of Homo Sapiens anti-Mullerian hormone (AMH) digested by Plasmin from human plasma on endometriosis stromal and epithelial cell line. (A) Epacadostat research buy pre-G1 fraction analysis of endometriosis stromal cells treated for 24-48-72 hrs with the final concentrations of cleaved MIS as indicated. The data are shown in a time-dependent manner. (B) pre-G1 fraction analysis of endometriosis stromal cells treated for 24-48-72 hrs with the final concentrations of cleaved MIS as indicated. The data are shown in a dose-dependent manner. (C) Cell cycle analysis of endometriosis stromal cells treated for 24-48-72 hrs with the final concentrations of cleaved MIS as indicated. The data are shown in a time-dependent manner. (D) Cell cycle analysis of endometriosis stromal cells treated for 24-48-72 hrs with the final concentrations of cleaved MIS as indicated. The data Selleckchem GDC-0994 are shown in a dose-dependent manner. (E) pre-G1 fraction analysis of endometriosis epithelial cells treated for 24-48-72 hrs with 1000 ng/mLof cleaved MIS. The data are shown in a time-dependent manner.

(F) Cell cycle analysis of endometriosis epithelial cells treated for 24-48-72 hrs with 1000 ng/mLof cleaved MIS. The data are shown in a time-dependent manner. Discussion Endometriosis is a benign disease of women during reproductive age [17];

nevertheless, it is well known that endometriosic cells display functional properties that are typical of neoplastic cells, such as MycoClean Mycoplasma Removal Kit anti-apoptotic, invasive and metastatic capacities [18, 19]. In support to this observation, epidemiological studies have shown that there exists an increased risk of different types of malignancies, especially ovarian cancer and non-Hodgkin’s lymphoma in women with endometriosis [20, 21]. Nevertheless, it has been reported an association between endometriosis, dysplastic nevi, melanoma, and breast cancer [22, 23]. Finally, several histological and genetic studies have indicated that endometriosis may transform into cancer or that it could be considered a precursor of cancer [24]. Recently, it has been demonstrated by Wang et al., that adult human endometrium has a functional AMH/AMHRII signal transduction system and that the activation of this system is able to negatively regulate cellular viability in cultured endometrial cells [12]. Indeed, the exact biological role of AMH in adult females is unclear. The most well recognized function in adult is its involvement in recruitment and selection of initial primordial follicles [25]. In fact, there exists a plethora of research articles on the use of AMH serum level as a sensitive marker to assess the ovarian reserve [26].

and the pellets suspended in 0.85% NaCl (OD600 = 1.0). The bacterial suspensions were separately mixed with sterilized activated charcoal (4:6 v/w) to give a CFU of approximately 107/g

of charcoal-based bacterial inoculants. Plant growth under controlled environment Seeds of Zea mays var. Girija surface sterilized with 20% sodium hypochlorite for 3 min. and washed thrice with sterile distilled water were germinated at 25°C in moist sterile vermiculite. Uniformly germinated seeds were coated with the Fosbretabulin supplier water slurry of charcoal-based microbial inoculants (approx. 5 × 105 CFU/seed) and two seeds per pot sown in 15 cm diameter pots filled with 2 kg non-sterilized sandy-loam soil. The soil used had pH 6.96, organic matter 3.1%, available N 0.03%, available P 0.0011%, available K 0.013% and available Ca 0.028%. The germinated seeds treated with the water slurry of sterilized SCH772984 concentration activated charcoal without inoculum were used for the control treatments. N and K were applied in the form of ammonium sulfate @ 240 kg N/ha, and muriate of potash @ 80 kg K/ha, respectively. P was applied @ 120 kg P/ha either as single super phosphate (SSP) or tricalcium phosphate (TCP) according to the various treatments. The phosphate-solubilizing bacterial (PSB) treatments included one P. fluorescens strain, three P. poae strains, ten P. trivialis strains, and five Pseudomonas spp. strains in combined application

with NPK with TCP as the phosphate source. TCP was chosen as phosphate substrate since P-deficiency in soils of the cold deserts of Lahaul and Spiti is attributed mainly to the presence of insoluble di- and tricalcium phosphates. The influence of PSB treatments on plant growth and soil properties was evaluated in comparison to the uninoculated control treatments with or without TCP and SSP. The pots were placed in a complete randomized block design with four replications under 550 μM photon m-2

s-1 mixed incandescent and fluorescent ABT-263 price illumination, 16/8 h light/dark cycle and 50–60% RH at 25 ± 2°C in an Environment Control Chamber. The plants were removed carefully under a gentle flow of tap water after 90 days of sowing. Data on root length, plant height (aerial parts), root dry weight Dimethyl sulfoxide and shoot dry weight were recorded. The samples were oven-dried at 70°C for 3 days to a constant weight for determining the dry weight. Chemical analyses The soil samples were air dried and sieved for determining pH, available N, P, K, Ca and organic matter content. The plant samples were oven-dried and powdered for estimation of total N, P and K. Organic matter was determined by the modified Walkley and Black method [12]. Estimation of total N was done by modified Kjeldahl’s method, total P by vanado-molybdate yellow colour method, total and available K by flame photometric method, and available Ca in ammonium-acetate extracts [13].

Further basic studies will elucidate the mechanisms underlying lymphatic metastasis. Meanwhile, in the clinical Selleck DMXAA field, lymph node metastasis offers an important prognostic factor for gastrointestinal (GI) cancer. The presence of tiny lymph node metastasis, in the form of lymph node micrometastasis (LNM) that is not detectable by routine histological examination, has been reported in carcinomas of various organs. Although overt lymph node metastasis is thought to be related to prognosis, what is

the relationship between LNM and prognosis? Recent advances in techniques such as immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR) have allowed the detection of LNM. Recently, LNM has been defined by the criteria of TNM classification and roughly divided in some categories according to the size of the metastatic foci or the method of detection. Clinical evaluation of LNM is somewhat difficult, because of the differences in study designs and methods of detection, such as the sample size, Trichostatin A chemical structure tumor stage of patients, number of removed nodes based on the area of lymph node dissection, use of immunohistochemistry, RT-PCR, or other methods, and the kinds of antibodies or primers used. Several EPZ004777 concentration articles have discussed

the clinical significance of LNM of GI cancer. The present review articles summarize the current knowledge of LNMs in GI cancer from the perspectives of both molecular and Amrubicin biological

characteristics and clinical aspects. These articles will be helpful as an overview of the current understanding of LNM and areas requiring further investigation. Conflict of interest The author declares that he has no conflict of interest.”
“To the editor, We read with great interest the study by Karita and colleagues [1] on the efficacy of caffeine-potentiated chemotherapy in clear cell sarcoma. The authors are to be congratulated for publishing promising data on a rare disease. However, several points should be clarified for the benefit of readers. The response rate to chemotherapy cannot be assessed in the adjuvant setting. The quoted study by Kuiper et al. [2] did not report a response rate of 25% (1 out of 4 patients), as these investigators treated 3 patients with adjuvant chemotherapy. Furthermore, the authors state that chemotherapy has “little impact” on survival with overall survival rates of 55–68%. No comment can be made on the effect on survival of adjuvant chemotherapy from these retrospective studies and case reports in such a rare disease. The authors state that “it is generally thought that chemotherapy results in poor response and survival” in clear cell sarcoma, but do not reference this statement.

It is therefore necessary that a more independent Selleck GSI-IX research on the overall health risk associated with nanoproducts be made very transparent and available to all concerned. In light of this, various governments of the world should consistently encourage nanotechnology health risk research as it may concern them with adequate funding to achieve objective results within an objective and proper legislative framework. LDC and African nations in particular should urgently review her tertiary education programs to give the much desired attention to nanomaterials testing, synthesis, and characterization using state-of-art equipment; otherwise they may be promoting

the much talked about ‘nano divide’ of which they will suffer more as consuming nations. The time to act is now. Finally, African nations click here and LDC

should endeavor to utilize the window of cooperation and collaboration now available with developed countries such as USA, European Commission, China, and Japan to enable them to access assistance. This ATM/ATR targets assistance may be sorted through proper training of her human capacity and funding/donation of equipment from these developed nations and multinational agencies which is specifically meant for nations at the demonstration of interest stage. This very window is wide open now but will not remain so for a long time. African nations and other LDC should not allow such opportunity to waste Chlormezanone away. The earlier they make advances to the realities of nanotechnology, the better their nations will be. It is only when these steps are taken that African nations and other LDC can apply nanotechnology innovatively to improve the quality of life of her citizens, thus enabling local industries and businesses to strive for sustainability and competitiveness in today’s global business setting. The emphasis is on PPP and networking through responsible development and regulatory framework by all government ministries, agencies, and stakeholders. We are calling

on the laboratories of the developed countries and the BRIC to urgently take up these challenges of the developing countries if our dream of global integration is to be real. The time for this assistance is now. Acknowledgements Our appreciation goes to Biomed Central and Springer Open waivers for granting waiver on the processing charges for this manuscript. References 1. Butt NM: Nanotechnology and why for developing countries. In Presentation at a Workshop on Nanoscience and Catalysis (NSC): 2008 March 24–25; Islamabad. Department of Physics Qaudi-i-Azam University; [http://​www.​ncp.​edu.​pk/​docs/​wnsc_​2008/​24-03-08/​Dr_​N_​M_​Butt.​pdf] 2. Abraham T: Nanotechnology & nanomaterials – applications and global market analysis. [http://​www.​aibn.​uq.​edu.​au/​Download/​NSF/​Thomas_​Abraham_​iRAP.​pdf] 2012. 3. Rao CNR, Govindaraj A: Nanotubes and nanowires. Proc Indian Acad Sci (Chem Sci) 2001,113(5 & 6):375–392.

Here, we investigate the invasion of spatially structured habitats by two separate populations in microscopic detail. Time-lapse fluorescence microscopy of two differentially labeled strains Eltanexor in vitro of E. coli allows us to resolve dynamics within the interacting populations down to the single cell level. In order to approximate the natural patchy environment of bacteria, we make use of microfabrication to create spatially structured habitats, PD0332991 order consisting of coupled arrays of habitat patches. We focus on three related questions (i) how are these patchy habitats colonized? (ii) how do the two strains

invading from opposite ends of the landscape interact during the colonization of the habitat? and (iii) how reproducible are the colonization patterns? We found that cells colonize a habitat from opposite sides by a series of traveling waves followed by an expansion front. The populations invading from opposite ends do not mix in the habitat, rather, colonization waves collide and expansion fronts compete for the landscape. We demonstrate that these interactions are mediated by diffusible chemicals. We found that the qualitative features of the colonization patterns are similar

for all experiments, even though population distributions vary widely between experiments. However, when parallel habitats located on the same device are inoculated LY2109761 datasheet from the same initial cultures, we observe strikingly similar

population distributions. Results Using microfabrication we created devices consisting of five parallel habitats, each consisting of an array of 85 patches connected by buy Forskolin narrow connectors (Figure 1A-C). Habitats are connected to either individual inlets (type 1 devices, Figure 1A), or to a single shared inlet (type 2 devices, Figure 1B) used for inoculation. Unless noted otherwise, two differentially labeled, but otherwise isogenic, strains of E. coli were inoculated at opposite sides of the habitats. We refer to cells and populations of these strains as ‘green’ (strain JEK1036) and ‘red’ (strain JEK1037). The neutrality of the two markers was demonstrated in previous work [42] and verified here by measuring growth in bulk conditions (see Methods and Additional file 1). Figure 1 Colonization of spatially structured synthetic ecosystems. (A) Device of type-1 with 5 parallel habitats (habitats 1 to 5 from top to bottom), each consisting of 85 patches, with separate inlets. Red cells are inoculated on the right (indicated by red inlet holes) and green cells on the left (green inlet holes). (B) Device of type-2 with a single, shared, inlet. Except for the inlet, devices in A and B are identical. (C) Enlarged schematic view of the devices shown in A and B showing an array of patches of 100 × 100 × 5 μm3 linked by connectors of 50 × 5 × 5 μm3.