Autocrine Go6983 VEGF inhibition using a VEGF trap strongly increased in interphase microtubule dynamic instability (+ 43%). Consistently, exogenously added VEGF (10 ng/ml) suppressed microtubule dynamic instability (− 29%). Interestingly, the suppression of microtubule dynamics occurred through their plus end stabilisation at paxillin-containing focal adhesions. Moreover, VEGF increased EB1 comet length at microtubule plus end by 32 %, without any change in its expression level. Differential post-translational modifications of EB1 were detected by 2D electrophoresis and western blotting. Their characterizations are under investigation

by mass spectrometry. In conclusion, our results show (i) that microtubules integrate signals from the tumor microenvironment, (ii) that VEGF and MTA have opposite effect on microtubule and EB1 dynamics

supporting the clinical benefit of the therapeutic combination of VEGF inhibitors and MTA, and (iii) suggest a potential role of EB1 protein in angiogenesis. 1- Pasquier E, et al Cancer Res 2005. 2- Pourroy B, et al Cancer Res 2006. 3- Honoré S, et al buy ABT-737 Mol Cancer Ther.2008. Poster No. 193 3D Models to Track Endothelial Progenitors to a Tumor Site Application to In Vivo Imaging of Cell Migration Krzysztof Szade1,2, Witold Nowak1,2, Catherine Grillon1, Nathalie Lamerant-Fayel1, Alan Guichard1, David Gosset1, Alicja Jozkowicz2, Jozef Dulak2, Claudine Kieda 1 1 selleck Centre de Biophysique Moléculaire, UPR 4301, CNRS, Orléans, France, 2 Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics

and Biotechnology, Kraków, Poland Tumor angiogenesis is crucial to support tumor cells growth and allow them to form metastasis [1]. Endothelial progenitor cells (EPC) are key players that influence tumor neovascularisation being directly incorporated into the tumor vessels [2]. Subsequently, we use progenitors of endothelium as vehicles for killer genes to be expressed preferentially in tumors [3]. This needs to determine the chemokines network that guides the progenitor and stem cells toward tumor. Here, we study mice model of melonama (B16F10 cells) and primitive endothelial precursors Carbohydrate isolated from mice embryo (MAgEC – Murine Aorta-gonad-mesonephros Endothelial Cells). To investigate the potential of B16F10 cells to stimulate MAgECs migration we applied two in-vitro methods with usage of fluorescence and pseudo confocal video microscopy, applied to dynamic phenomena using shear stress conditions and time lapse measurements on long term experiments. The first method was based on transwell inserts and visualization of MAgEC invasion through Matrigel. In the second one, 3D tumor spheroids were formed and migration of MAgEC through collagen gel towards spheroids was investigated. This allows to study the chemokine activity as we showed that CCL21 augments MAgEC sensitivity and migration potential. Such “education” may be important in cell based therapy against tumor.

coli BL21DE3/pBJN406 grown on TSA plates in the presence of 0.5, 1.5, 2.5 and 3.5 mM of agents 1 and 2, respectively. In the experiments presented by M and N panels the E. coli BL21DE3/pBJN406 strain was grown in the presence of 3.5 mM of pilicides. The selleck chemicals Figure presents representative results obtained from

three independent experiments. Each experiment was composed from the four-fold repetition for each used bacterial preparation. The bacterial adherence to 40 CHO cells was determined for each repetition. Presented Alvocidib in the figure pilicides 1 and 2 are the literature agents which, at a 3.5 mM concentration, inhibit the assembly of FGS type 1 and P pili. Pilicides block Dr fimbriae-dependent bacterial adherence At the first stage, we determined

the adherence of bacteria cultivated on TSA plates in the presence of 0.5, 1.5, 2.5 and 3.5 mM of pilicides 1 and 2 to the CHO cells transfected with plasmid encoding DAF receptor protein recognized by Dr fimbriae. The process of bacteria attachment was visualized by means of Giemsa staining. In the case of strain BL21DE3/pBJN406 cultivated without pilicide (positive control), we observed a high level of bacteria attachment to the CHO-DAF+ cells related to the undisturbed production of Dr fimbriae (Figure 1I). The adherence of positive control is set as 100% ±12 and the observed adherences of all other used bacterial preparations are expressed as the percentage of mean value of adherence present relative to control. The addition of 3.5 mM

pilicide to the bacterial growth media resulted in a very high reduction check details in the bacterial adhesion properties: for pilicide 2, only a few bacterial cells were visible as attached, corresponding to the relative bacterial adherence of 13% ±3 (Figure 1B) and for pilicide 1 resulted in a slightly lower inhibition of bacterial attachment, corresponding to the relative adherence of 25% ±7 (Figure 1A). E. coli BL21DE3/pBJN406 bacterial strains cultivated in the presence of 0.5, 1.5 and 2.5 mM of pilicides 1 and 2 showed dose dependent relative adherence of: 90% ±3, 60% ±5 and 32% ±6 for pilicide 1 and 92% ±8, 42% ±7 and 21% ±9 for pilicide 2, respectively (Figure 1 G,E,C and H,F,D). In order to confirm that the bacterial adherence is dependent on the specific interactions between the DraE MYO10 fimbrial subunits and DAF, we used as the control non-transfected CHO cells, which do not express DAF molecules naturally. The relative adherence of Dr-fimbriated BL21DE3/pBJN406 positive control (Figure 1J), non-fimbriated BL21DE3/pACYC184 negative control (Figure 1L) and BL21DE3/pBJN406 strain grown in the presence of 3.5 mM of pilicide 1 or 2 (Figure 1M and N) to the CHO-DAF- cells for all experiments was of 3-6% ± 1–2. The similar value of relative adherence of 5% ±6 was determined for binding of non-fimbriated BL21DE3/pACYC184 negative control strain to CHO-DAF+ cells.

All authors read and approved the final manuscript.”
“Background Hepatocellular carcinoma (HCC) is the fifth most common malignant tumor worldwide, with over 600,000 new cases diagnosed each year, and buy AZD1080 is the third most common tumor-related cause of death [1]. Hepatitis B virus (HBV) infection, hepatitis C virus infection, and aflatoxin-induced oncogene activation and tumor suppressor gene inactivation are the main

causes of HCC [2]. Surgical resection and liver transplantation may cure HCC, but about 85% of patients have locally advanced tumor or distant metastasis at the time of diagnosis, and are not suitable candidates for surgery [3]. Conventional chemotherapy for HCC has limited effectiveness, but recent breakthroughs in treatment with molecular-targeted drugs have been reported. Abnormalities of intracellular signaling pathways which result in abnormal cell proliferation and apoptosis are one of the main mechanisms of HCC development. 3-MA solubility dmso Many complex cellular signaling pathways are

involved in tumor development and growth. These pathways include proteins such as vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR), platelet-derived growth factor (PDGF), PDGF receptor (PDGFR), hepatocyte growth factor/c-Met, Ras/Raf/Mek/Erk, and PI3k/Ak/mTOR. High expression of VEGFR-2, PDGFR-β, and c-Met can be detected in many tumors, including HCC, but information regarding the relationships between expression of VEGFR-2, PDGFR-β, and c-Met and the clinicopathological factors and prognosis of HCC is very limited [4–7]. This study explored the relationships between expression of VEGFR-2, PDGFR-β, and c-Met and the clinicopathological factors and prognosis of HCC patients, aiming to provide AZD1152 ic50 reference information to assist with the diagnosis, evaluation of prognosis, and targeted therapy of HCC. Methods Specimens were collected from 93 HCC patients treated at the Department of Digestive Oncology, Chinese People’s Liberation Army 307 Hospital from January

2007 to October 2011. The specimens were collected from patients by biopsy and it was excluded Ixazomib purchase if the biopsy specimen was too less. Sixty-five of these patients were taking sorafenib. All patients met the following inclusion criteria: (1) advanced stage HCC which was not suitable for surgery or local treatment, or had recurred after surgery or local treatment, (2) Child-Pugh class A or B, (3) Eastern Cooperative Oncology Group (ECOG) score 0 or 1, (4) at least one target lesion that had not been previously treated, (5) no local treatment for at least 4 weeks before baseline imaging, (6) availability of complete clinical and pathological data, including follow-up data. All specimens were fixed in 10% formaldehyde, embedded in paraffin, and cut into 4-μm thick slices before staining.

by BMBF is gratefully acknowledged. References Adelin check details E, Servy C, Cortial S, Lévaique H, Martin M-T, Retailleau P, Goff GL, Bussaban B, Lumyong S, Ouazzani J (2011) Isolation, structure elucidation and biological activity of metabolites from Sch-642305-producing endophytic fungus Phomopsis sp. CMU-LMA. buy OSI-744 Phytochemistry 72:2406–2412PubMed Ahmed I, Hussain H, Schulz B, Draeger S, Padula D, Pescitelli G, van Ree T, Krohn K (2011) Three new antimicrobial metabolites from the endophytic fungus Phomopsis sp. Eur J Org Chem 2867–2873 Almeida C, Kehraus S, Prudêncio M, König GM (2011) Marilones A-C, phthalides from the sponge-derived fungus Stachylidium

sp. Beilstein J Org Chem 7:1636–1642PubMed Aly AH, Debbab A, Kjer J, Proksch P (2010) Fungal endophytes from higher plants: a prolific source of phytochemicals

and other bioactive natural products. Fungal Divers 41:1–16 Aly AH, Debbab A, Clements C, Edrada-Ebel RA, Orlikova B, Diederich M, Wray V, Lin WH, Proksch P (2011a) NF kappa B inhibitors and antitrypanosomal metabolites from endophytic fungus Penicillium sp. isolated from Limonium tubiflorum. Bioorg Med Chem 19:414–421PubMed Aly AH, Debbab A, Proksch P (2011b) Fungal endophytes: unique plant inhabitants with great promises. Appl Microbiol Biotechnol 90:1829–1845PubMed Amann RL, Ludwig Paclitaxel in vivo W, Scheidler KH (1995) Phylogenetic identification and in situ detection of individual microbial cells without cultivation. FEMS Microbiol Rev 59:143–169 Arnold AE, Mejia LC, Kyllo D, Rojas EI, Maynard Z, Robbins N, Herre EA (2003) Fungal endophytes limit pathogen damage in a tropical tree. Proc Nat Acad Sci USA 100:15649–15654PubMed Ball OJ, Gwinn KD, Pless CD, Popay AJ (2011) Endophyte isolate and

host grass effects on Chaetocnema pulicaria (Coleoptera: Chrysomelidae) aminophylline feeding. J Econ Entomol 104:665–672PubMed Baltruschat H, Fodor J, Harrach BD, Niemczyk E, Barna B, Gullner G, Janeczko A, Kogel KH, Schäfer P, Schwarczinger I, Zuccaro A, Skoczowski A (2008) Salt tolerance of barley induced by the root endophyte Piriformospora indica is associated with a strong increase in antioxidants. New Phytol 180:501–510PubMed Barrow JR, Lucero ME, Reyes-Vera I, Havstad KM (2008) Do symbiotic microbes have a role in plant evolution, performance and response to stress? Commun Integr Biol 1:69–73PubMed Bergmann S, Schumann J, Scherlach K, Lange C, Brakhage AA, Hertweck C (2007) Genomics-driven discovery of PKS-NRPS hybrid metabolites from Aspergillus nidulans. Nat Chem Biol 3:213–217PubMed Blume B, Nürnberger T, Nass N, Scheel D (2000) Receptor-mediated increase in cytoplasmic free calcium required for activation of pathogen defense in parsley. Plant Cell 12:1425–1440PubMed Blunt JW, Copp BR, Keyzers RA, Munro MHG, Prinsep MR (2012) Marine natural products. Nat Prod Rep 29:144–222PubMed Bode HB, Bethe B, Höfs R, Zeeck A (2002) Big effects from small changes: possible ways to explore nature’s chemical diversity.

Serum samples were unavailable for both members of 2 pairs. Zygosity was confirmed by genotyping 46 single nucleotide polymorphisms using two Sequenom iPlex panels. The analysis sample consisted of 45 pairs of rigorously discordant and genetically proven monozygotic twins. Discordance was defined as one twin meeting criteria for either idiopathic chronic fatigue (ICF, 13 pairs) or CFS (32 pairs) [1, 2] and the co-twin was required never to have experienced impairing unusual https://www.selleckchem.com/products/Cyt387.html fatigue or tiredness lasting more than one

month. Thus, all affected twins were required to have current, long-standing (≥6 months), medically unexplained fatigue associated with substantial impairment in social and occupational functioning and the unaffected co-twins were effectively well. Biological sampling Biological sampling was standardized by having samples drawn from both members of a twin pair at the same place and time (~0900) after an overnight fast. We required that all subjects be in their usual state of health on the day of sampling (i.e., no acute illness or recent exacerbation of a chronic illness). It was neither practical nor ethical to study subjects medication-free,

but we delayed assessment if there had been a recent significant Selleck MK-4827 dosage change. Peripheral venous blood was drawn using sterile technique. Viral library preparation and sequencing Serum samples from 45 pairs of affected

and unaffected monozygotic twins were available for this study. Sample preparation for library construction was as described previously [14] and, briefly, consists of viral particle recovery and nucleic acid extraction, followed by amplification and cloning of viral nucleic acid. Serum samples (200 μl) from the affected twins were pooled separately from their unaffected co-twins. Serum pools were then filtered either through 0.22 μm or 0.45 μm membrane filters (Millipore) and virus particles were concentrated by ultracentrifugation (41,000 rpm for 1.5 h at 4°C in a Beckman SW41 rotor). Exogenous nucleic acids were removed by DNaseI and RNaseA treatment followed by extraction of viral DNA (Qiagen) or RNA (Trizol, selleck chemicals llc Invitrogen). First strand synthesis was carried out with Hydroxychloroquine mouse a random primer containing an EcoRV site plus exonuclease negative Klenow polymerase (Promega) for DNA and Superscript II reverse transcriptase (Invitrogen) for RNA. Second strand synthesis for the above reactions was carried out with exonuclease negative Klenow polymerase (Promega). These were then amplified with AmpliTaq Gold polymerase (Applied Biosystems) and a primer complementary to part of the random primer used in first strand synthesis. PCR products were purified, digested with EcoRV, subjected to gel electrophoresis, and bands 500 bp – 5 kb were extracted from the gels.

The pTAP and pTP constructs were introduced into E.

coli DH5α by electroporation using a Gene Pulser (BioRad) with settings of 2.5 kV and 25 μF. Recombinants were selected for ampicillin resistance and clones were screened for the presence of the gentamicin resistance gene using the oligonucleotide primers GmF and GmR. Selected clones were cultured in larger volumes and plasmid DNA extracted using a Midi prep kit (Qiagen) according to the manufacturer’s instructions. Transformation of M. gallisepticum M. gallisepticum was transformed by electroporation as described previously [39, 40]. Following electroporation, cells were gently resuspended in 1 ml of ice-cold MB, incubated at 37°C to allow expression of the gentamicin resistance selleck compound gene, then a 500 μl aliquot of the culture inoculated onto MA plates containing 16 μg of gentamicin/ml, which were allowed to dry and then incubated at 37°C for 4 days. The plates were examined

for colony development and single colonies selected and subcultured in MB containing 16 μg of gentamicin/ml. Detection of alkaline phosphatase activity on MA plates To detect alkaline phosphatase activity in colonies of transformed M. gallisepticum on MA plates, a single tablet of BCIP/nitroblue tetrazolium (NBT) (Sigma Fast, Sigma) was dissolved in 3 ml distilled water and sprayed onto the colonies uniformly as a thin layer using a pump atomizer. After 10 min colonies were observed for the presence of a blue colour. Genomic DNA sequencing To determine the insertion site of the transposon, genomic DNA very sequencing was carried out Torin 1 using the ABI Prism BigDye Terminator v3.1 (BDT) sequencing system (Perkin Elmer Applied Biosystems) and the UBR oligonucleotide primer (Table 1) according to the manufacturer’s instructions, with minor modifications. Approximately 2 μg of genomic DNA was combined with 1 μM of the UBR oligonucleotide, 4 μl of the

BDT enzyme mixture, 4 μl of 5 x BDT buffer and distilled water to 20 μl. The sequencing reaction LOXO-101 mixture was incubated at 96°C for 5 min, then through 60 cycles of 96;°C for 30 s, 50°C for 10 s and 60°C for 4 min in an iCycler thermocycler (BioRad). The sequencing products were purified according to the manufacturer’s instructions using ethanol-EDTA-sodium acetate precipitation and analysed using an ABI3100 capillary sequencer. Quantitative RT-PCR Quantitative RT-PCR (qRT-PCR) was used to determine the level of transcription of the phoA gene in each of the transformants. To achieve this, total RNA from 6 ml of transformant cells was extracted using an RNA purification kit (Qiagen), following the manufacturer’s instructions. The total amount of RNA was determined using an ND-1000 spectrophotometer (NanoDrop). To remove any contaminating DNA, 2 μg of extracted RNA was treated with 2 U of DNase I (Invitrogen) in a buffer containing 2 μl of 10 x DNase I buffer and RNase-free water in a total volume of 20 μl for 15 min at room temperature.

Then, 1 ml of THF and saturated solution of NH4Cl (10 ml) were GS-1101 added and the whole mixture was extracted with CH2Cl2 (3 × 5 ml). The 1H NMR and IR spectroscopic data were in agreement with those reported in the literature (Cano et al., 2006; NSC 683864 in vivo Siddiqui et al., 2003). 1H NMR (300 MHz, acetone-d 6) δ (ppm): 0.93 (t, 3H, J = 7.3 Hz, C-7–O(CH2)4CH3); 1.41 (m, 2H, C-7–O(CH2)3CH2CH3); 1.49 (m, 2H, C-7–O(CH2)2CH2CH2CH3); 1.61 (d, 6H, J = 1.4 Hz, CH3-4′′ and CH3-5′′); 1.82 (m, 2H, C7–OCH2CH2(CH2)2CH3); 2.79 (dd, 1H, J = 17.0 Hz, J = 3.0 Hz, CH-3); 3.16 (dd, 1H, J = 17.0 Hz, J = 12.6 Hz, CH-3); 3.22 (d, 2H, J = 7.2 Hz, CH2-1′′); 4.08 (t, 2H, J = 6.3 Hz, C-7–OCH2(CH2)3CH3); 5.15 (t sept, 1H, J = 7.2 Hz, J = 1.4 Hz,

Roscovitine purchase CH-2′′); 5.46 (dd, 1H, J = 12.6 Hz, J = 3.0 Hz, CH-2); 6.12 (s, 1H, CH-6); 6.90 (d, 2H, J = 8.5 Hz, CH-3′ and CH-5′); 7.41 (d, 2H, J = 8.5 Hz, CH-2′ and CH-6′); 8.51 (s, 1H, C-4′–OH); 12.24 (s, 1H, C-5–OH). C25H30O5 (410.51): calcd. C 73.15, H 7.37; found C 73.32, H 7.54. 7,4′-Di-O-allyl-8-prenylnaringenin (13) Yield 78.9%, mp = 103–105°C,

R f = 0.84 (CHCl3:MeOH, 99.3:0.7), pale yellow solid. 1H NMR (300 MHz, acetone-d 6) δ (ppm): 1.60 (d, 6H, J = 1.3 Hz, CH3-4′′ and CH3-5′′); 2.82 (dd, 1H, J = 17.1 Hz, J = 3.1 Hz, CH-3); 3.18 (dd, IMP dehydrogenase 1H, J = 17.1 Hz, J = 12.5 Hz, CH-3); 3.24 (d, 2H, J = 7.2 Hz, CH2-1′′); 4.59 and 4.65 (two ddd, 4H, J = 5.1 Hz, J = 1.7 Hz, J = 1.5 Hz, C-7- and C-4′–OCH2CH=CH2); 5.16 (t sept, 1H, J = 7.2 Hz, J = 1.3 Hz, CH–2′′); 5.23–5.31 (m, 2H, trans-C-7- and trans-C-4′–OCH2CH=CH2); 5.51 (dd, 1H, J = 12.5 Hz, J = 3.1 Hz, CH-2); 5.39–5.48 (m, 2H, cis-C-7- and cis-C-4′–OCH2CH=CH2); 6.02–6.16 (m, 2H, C-7- and C-4′–OCH2CH=CH2); 6.12 (s, 1H, CH-6); 7.02 (d, 2H, J = 8.8 Hz, CH-3′ and CH-5′); 7.50 (d, 2H, J = 8.8 Hz, CH-2′ and CH-6′). IR (KBr) cm−1: 2967, 2911, 2857, 1636, 1587, 1517, 1448, 1378, 1255, 1178, 1118, 1021, 921, 829. C26H28O5 (420.51): calcd. C 74.26, H 6.71; found C 74.09, H 6.88. 7,4′-Di-O-acetyl-8-prenylnaringenin (14) Yield 88.4%, mp = 139–140°C, R f = 0.84 (CHCl3:MeOH, 98:2), white solid.

2/100.000 inhabitants. Current scope of practice There are 5 medical schools built around university AZD7762 nmr hospitals in Finland. In the multi-layered public health care system, primary care is provided by the healthcare centers in each of the about 400 counties. For Selleckchem Bioactive Compound Library specialist care, Finland is divided into 21 hospital districts.

There are 5 university hospitals and 16 central hospitals that provide most of the specialist care including surgical emergency services in their respective areas. There are also some, smaller district hospitals where basic surgical services are provided. The 5 university hospitals have special responsibilities for the most demanding specialized care in their area, and in some cases, such as transplantation surgery or major burn care, the centralization goes even further to one or two centers in the whole country. Overall, about 400.000 surgical procedures are performed each year in the public hospitals. In addition, there are private hospitals mostly in larger cities providing elective surgical services with SN-38 ic50 varying degree of specialization. The majority of patients with emergency surgical problems are managed in the university and central hospitals, although certain specialist services, such as cardiothoracic and neurosurgery, are available almost exclusively in university hospitals. In most central hospitals, there are usually one or

two surgical residents on call in the hospital outside the working hours with more senior surgeons (one Methamphetamine general or “”visceral”", and one orthopedic surgeon) on call at home with a response time obligation of 30 minutes at the most. The university hospitals have usually in-house specialist surgeons from the large specialties (gastroenterological surgery, orthopedics and traumatology) available around the clock and on-call services from home of other specialties including urology, vascular surgery, pediatric surgery, plastic surgery etc. Most of the emergency general surgery (mainly acute

abdomen) is performed by gastroenterological surgeons or residents, but in smaller hospitals also other visceral surgeons (urologists or vascular surgeons, for example) participate in the on-call rosters. Same applies to abdominal trauma including damage control surgery, whereas vascular or thoracic trauma patients are usually referred to a center with vascular surgeons or thoracic surgeons on-call, respectively. Intensive care is largely provided by anesthesiologists with special interest in intensive care. Intensive care is not part of the surgical training curriculum. Current training program In the past, all surgeons were trained as general surgeons (including orthopedic surgery) for 6 years. If desired, an additional two-year fellowship in some specialized field (gastroenterological surgery, urology, plastic surgery, orthopedic surgery etc.) could be taken leading to a subspecialty in that field.

This richness is considerably higher than the 34 to 72 phylotypes and the 6 to 30 genera previously described using conventional cloning and sequencing [15, 16]. The predominant taxa belonged to Firmicutes (genus Streptococcus, family Veillonellaceae, genus

Granulicatella), Proteobacteria (genus Neisseria, Haemophilus), Actinobacteria (genus Corynebacterium, Rothia, Actinomyces), Bacteroidetes (genus Prevotella, Capnocytophaga, Porphyromonas) and Fusobacteria (genus Fusobacterium) (Additional file 4). Figure 2 The relative abundance of OTUs per individual. Relative abundance of OTUs based on all unique sequences (0%, solid lines) and OTUs within genetic distances that do not exceed 3% difference (3%, dashed lines) per individual S1, S2 and S3, respectively. The x-axis indicates the individual OTUs, ranked according to their relative abundance (high find more to low). The y-axis indicates the cumulative abundance of the OTUs. About 100 “”species-level”" phylotypes (118, 97 and 112 phylotypes in the microbiome of individual S1, S2 and S3, respectively) belonged to abundant OTUs of the individual microbiome (Additional file 1). A phylotype was considered abundant if it contributed to at least 0.1% of the microbiome. These abundant phylotypes together contributed to 92 – 93% of each microbiome. As with a pooled oral microbiome [4] and

individually NSC 683864 ic50 sequenced gut microbiomes [13], each individual oral microbiome in this study was dominated by a few sequences while most sequences were rare and contributed to the “”long tail”" effect (Figure 2). Overlap of three individual oral microbiomes Unique sequences Selleckchem GSK458 Twenty-six percent (1660 sequences) of the unique sequences were found in all three microbiomes and 65% in at least

two microbiomes (Figure 3A). Of all reads, 66% belonged to sequences that were shared by three microbiomes (Table 2). Nine sequences were highly abundant (0.5 – 5.8% of the reads) across all individuals: they contributed to 11%, 9% and 21% of the microbiome of individuals S1, S2 and S3, respectively (the full list of the taxonomy and abundance of the overlapping sequences is given in Additional file 5). Two of these sequences were assigned to the genus Streptococcus, two to the family Veillonellaceae, one each to the genera Granulicatella (Firmicutes), Corynebacterium, Rothia (Actinobacteria), Porphyromonas selleck (Bacteroidetes) and Fusobacterium (Fusobacteria). Figure 3 The extent of overlap of oral microbiome between three individuals. The extent of overlap between subjects S1 (pink circle), S2 (light blue circle) and S3 (yellow circle) at the level of A) unique sequences, B) OTUs clustered at 3% difference and C) higher taxa (genus or more inclusive taxon). The data was obtained by combining all samples of the respective individual microbiome. The Venn Diagrams show that 26% of the unique sequences, 47% of the OTUs and 72% of the higher taxa were common (area in grey) to the three individuals.

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