Acknowledgments We thank CME-UFRGS for confocal microscopy supply. This work was supported by CAPES-BRASIL/ESPANHA, FIPE-HCPA, UFCSPA. References 1. Pache I, Bize P, Halkic N, Montemurro M, Giostra E, Majno P, Moradpour D: [Management of hepatocellular carcinoma]. Rev Med Suisse 2010, 6:198–202.PubMed 2. Cervello M, Montalto G: Cyclooxygenases in hepatocellular carcinoma. World J Gastroenterol 2006, 12:5113–5121.PubMed 3. Jain S, Singhal S, Lee P, Xu R: Molecular genetics of hepatocellular neoplasia. Am

J Transl Res 2010, 2:105–118.PubMed 4. Hoshida Y, Toffanin S, Lachenmayer A, Villanueva A, Minguez B, Llovet J: Molecular Classification find more and Novel Targets in Hepatocellular Carcinoma: Recent Advancements. Semin Liver Dis 2010, 30:35–51.PubMedCrossRef 5. El-Bassiouni A, Nosseir M, Zoheiry M, El-Ahwany E, Ghali A, El-Bassiouni N: Immunohistochemical expression of CD95 (Fas), c-myc and epidermal growth factor receptor in hepatitis C virus infection, cirrhotic liver disease and hepatocellular carcinoma. APMIS 2006, 114:420–427.PubMedCrossRef 6. Nguyen H, Sankaran S, Dandekar

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treatment suppresses tumor growth but promotes metastasis capacity in hepatocellular carcinoma. J Cancer Res Clin Oncol 2010, 136:1891–1900.PubMedCrossRef Janus kinase (JAK) 9. Guo L, Guo Y, Xiao S: Expression of tyrosine kinase Etk/Bmx and its relationship with AP-1- and NF-kappaB-associated proteins in hepatocellular carcinoma. Oncology 2007, 72:410–416.PubMedCrossRef 10. Zingarelli B, Sheehan M, Wong HR: Nuclear factor-kappaB as a therapeutic target in critical care medicine. Crit Care Med 2003, 31:S105-S111.PubMedCrossRef 11. Dutta J, Fan Y, Gupta N, Fan G, Gélinas C: Current insights into the regulation of programmed cell death by NF-kappaB. Oncogene 2006, 25:6800–6816.PubMedCrossRef 12. Tas S, Vervoordeldonk M, Tak P: Gene therapy targeting nuclear factor-kappaB: towards clinical application in inflammatory diseases and cancer. Curr Gene Ther 2009, 9:160–170.PubMedCrossRef 13. Duan W, Jin X, Li Q, Tashiro S, Onodera S, Ikejima T: Silibinin induced autophagic and apoptotic cell death in HT1080 cells PRI-724 clinical trial through a reactive oxygen species pathway. J Pharmacol Sci 2010, 113:48–56.PubMedCrossRef 14. Luo J, Kamata H, Karin M: The anti-death machinery in IKK/NF-kappaB signaling. J Clin Immunol 2005, 25:541–550.PubMedCrossRef 15. Nakanishi C, Toi M: Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs. Nat Rev Cancer 2005, 5:297–309.PubMedCrossRef 16.

9)  Fixed-term contract 9 (2.9)  Temporary employment 4 (1.3)  Work hours per week [mean (SD)] 30 (6.3)  Mental health complaints 83 (26) Item reduction by explorative factor analysis As expected, all 231 items had a highly skewed distribution of answers. First, 19 items were deleted because of too little variance in answers. The data of all four clusters were suitable for the PCA. However, the PCA for the second cluster (causing incidents) had to be performed without the data of the allied health professionals, as too many “not applicable to my job” answers were given in https://www.selleckchem.com/products/SB-202190.html this group, leading to too many missing values.

The Kaiser–Meyer–Olkin values for the four clusters were 0.73, 0.72, 0.80, and 0.90, respectively; AZD3965 chemical structure all exceeding the recommended value of 0.60 (Kaiser 1970, 1974). Bartlett’s test of sphericity was significant in all cases (with P < 0.0001) (Bartlet 1954). Table 3 presents an overview of PCA PLX-4720 research buy Results and a description

of the content of the items included per selected factor. In the supplemented files, we present the rotated component matrix with the factor loadings for each cluster. Table 3 Results of the principal component analysis for all four clusters * Number of respondents who answered all items ** Percentage of variance explained by the first factor in each subscale *** This subscale is a selection of items from the subscale ‘causing incidents’ which are applicable to allied health professionals The PCA of the first cluster was performed with 82 items, of which 19 remained. Based on the scree-plot and the interpretability of the factors, a three-factor solution was chosen. It accounted for 32% of the explained variance. The following subscales were identified: “cognitive aspects of task execution”, “withdrawing from responsibilities”, and “impaired decision making”. The PCA of the second cluster was performed with 41 items, of which 15 remained.

An interpretable one-factor solution was chosen based on Ribose-5-phosphate isomerase the scree-plot, explaining 23% of the total variance. The identified subscale was “causing incidents at work”. For the third cluster, out of 61 items, 19 remained. The scree-plot of the PCA pointed to four factors, which were highly interpretable. It accounted for 36% of the overall variance. Subscale one is “avoiding contact with colleagues” and two is “conflicts and irritations with colleagues”. Subscale three and four are “impaired contact with patients and their family”; because of their overlap in underlying content, they were combined. In the PCA of the fourth cluster, with 28 items of which six remained, we chose the one-factor solution, based on the scree-plot and the good interpretability. It explains 35% of the variance. This subscale is called “lack of energy and motivation”. For each cluster, a final PCA was performed with the selected items. For all clusters, the selected number of factors was corroborated.

Fragments were PCR-amplified from SC5314 genomic DNA using the oligonucleotides listed in Table 3. The fragments were designed such that the entire coding sequence from ATG to the stop codon would be replaced by the SAT1 cassette. For both genes, the upstream fragment was cloned using the restriction enzymes ApaI and XhoI and the downstream fragment was cloned using NotI and SacII. To create the Candida albicans RAD54 reconstruction vector, the entire coding region, including promoter and terminator sequence was cloned into the ApaI-XhoI site in the Candida albicans RAD54 deletion vector. Table 3 List of oligonucleotides

RXDX-101 used in this study Oligonucleotide name 5′ – 3′ sequence CaRAD54upF CAACGTAGGGCCCTCTAAAAATGTTGAAATTGG CaRAD54upR CAACGTACTCGAGGAGAATGGAAAGTACTGT CaRAD54downF CAACGTAGCGGCCGCTTTTAATATAAAACAATGTTG CaRAD54downR CAACGTACCGCGGAGGAATACTTGCAGTTGAC CaRDH54upF CAACGTAGGGCCCATGTACAAGATAAATTTG CaRDH54upR CAACGTACTCGAGCGCGTTGACAAAATTC CaRDH54downF

CAACGTAGCGGCCGCCGCGTTTGACAAAATTC CaRDH54downR CAACGTACCGCGGCAAAAAGCACCAAAGTTG CaRAD54compR CAACGTACTCGAGAGGAATACTTGCAGTTGAC Restriction site RG7420 in vitro sequences are shown in bold Yeast transformation and screening SC5314 was transformed with linearized (linearized with ApaI and SacII) Candida albicans RAD54 or Candida albicans RDH54 deletion vectors using the standard lithium Selleckchem A-1210477 acetate method [34] with the following modifications. Heat shock at 42°C was carried out overnight, and cells were resuspended in YPD and allowed to grow for 4 hours at 30°C before plating on YPD containing 200 μg/mL cloNAT (Werner BioAgents, Jena, Germany). Recycling of the SAT1 marker was done by growing cells overnight in non-selective media (YPD) and plating onto YPD containing

25 μg/mL nourseothricin. Florfenicol Small colonies that had excised the marker were screened by PCR and used in a successive round of transformation. These tranformants were then screened by PCR for homozygous deletion of Candida albicans RAD54 and Candida albicans RDH54. To create the Candida albicans RAD54 reconstruction strain, recycling of the SAT1 marker was performed again and the reconstruction plasmid was introduced to the native locus by another round of transformation. Growth rate determination Overnight YPD cultures from three independent colonies were used to inoculate 3 mL YPD at an OD600 of 0.05. Cultures were grown at 30°C with shaking. OD measurements were taken every hour for 9 hours to generate growth curves. Doubling times of each strain were calculated using time points within the logarithmic phase of growth. This assay was repeated three times, the mean and standard deviations for each strain is shown. Colony morphology and microscopic analysis For assessment of colony morphology, cells were grown on YPD for 2 days at 30°C and single colonies were photographed. For colony invasion of agar, strains were streaked onto Spider agar plates (1% nutrient broth, 1% mannitol, 0.

CrossRef 10. Rutkowski S, De Vleeschouwer S, Kaempgen E, Wolff JE, Kuhl J, Demaerel P, Warmuth-Metz M, Flamen P, Van Calenbergh F, Plets C, Sorensen N, Opitz A, Van Gool SW: Surgery and adjuvant dendritic cell-based tumour vaccination for patients with relapsed malignant glioma, a feasibility study. Br J Canc 2004, 91:1656–1662. 11. Novoselov KS, Geim AK, Morozov SV, Jiang D, Zhang Y, Dubonos SV, Grigorieva IV, Firsov AA: Electric field effect in atomically thin carbon films. Science 2004, 306:666–669.CrossRef 12. Liu

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qE has been studied by researchers from a broad range of fields. This diversity of approaches has led to a wide variety of theoretical and experimental tools that have been valuable in studying qE. Fig. 1 To understand the mechanism of qE requires an understanding of the dynamics of the trigger, the membrane change, and the photophysical mechanism. The techniques CB-839 that are used to study the different aspects of the mechanism are listed below the respective process In this paper, we review the methods and techniques that have been used in qE research. These methods, though often developed and primarily used to study plants, can

be used to study qE in any photosynthetic organism, and many can be used to study any NPQ mechanism. We focus on the applications of these methods PF-562271 in vitro to samples that are capable of performing qE in response to light, such as thylakoids, chloroplasts, and whole leaves, and do not review many experiments done on isolated and aggregated proteins. For a review of experiments on isolated

complexes, see Ruban et al. (2012). We also limit the scope of this review to the application of these methods to qE in plants, although other organisms, such as cyanobacteria, also exhibit NPQ processes that have similarities with qE. Some methods, such as the use of fluorescence yield measurements, chemical inhibitors, and qE mutants, have been used to extract information about all parts of the qE process: the trigger, membrane change, and photophysical mechanism of quenching. We discuss the use of these methods, as well as their strengths and limitations, in the “General tools for the study of qE” section. In the “Triggering of qE” section, we discuss the current understanding of the trigger by reviewing methods and models for correlating qE with the lumen pH. We discuss the techniques used to monitor membrane changes and to identify the quenching site(s) and photophysical mechanism(s) of NPQ in the “Formation TCL of qE in the grana membrane” section. Finally, in the “New tools for characterizing

qE in vivo” section, we discuss the development of measurements and techniques to study the dynamics of qE in vivo. General tools for the study of qE Discovery and early studies of qE qE was first observed in fluorescence studies of isolated chloroplasts subjected to chemical treatments. The amount of chlorophyll fluorescence was found to depend on the pH of the lumen. Figure 3 illustrates the series of experiments performed by Murata and Sugahara (1969) and Wraight and Crofts (1970). Chloroplasts were first treated with NU7026 clinical trial dichlorophenyl-dimethylurea (DCMU), which inhibits electron transfer at PSII and prevents photochemical quenching. Because excited chlorophyll could not be quenched photochemically (by charge separation at the RC), a high level of fluorescence was observed.

Pycnidia (formed on WA on sterilized pine needles within 10 days) superficial on host surface, clustered in a stroma, multiloculate, globose to subglobose. Peridium comprising several layers of cells textura angularis, broader at the base, outer layers dark to dark-brown and thick-walled, inner layers hyaline and thin-walled. Conidiogenous cells (8-)10−14(−16) × 3–5 μm holoblastic, hyaline, cylindrical to Selleckchem GSK690693 ellipsoidal,

smooth-walled. Conidia (21-)22–25(−26) × 5–7 μm \( \left( \overline x = 23.5 \times 6\,\upmu \mathrmm,\mathrmn = 30 \right) \), hyaline, aseptate, cylindrical to cylindro-clavate, thin-walled, with rough wall. Culture characteristics: Colonies on PDA reaching 50 mm diam after 4 d at 25–30 °C, fast growing; circular, whitened in a few days, after one week becoming grey to green-black; flattened, Tozasertib concentration fairly dense, surface smooth with crenate edge, filamentous; reverse grey to black, pigments Milciclib cell line not produced in media. Material examined: THAILAND, Lampang Province, Jae Hom District, Mae Yuag Forestry Plantation, on dead culms of Bambusa sp., 19 August 2010, R. Phookamsak, RP0059 (MFLU11–0179, holotype), ex-type living culture MFLUCC11–0143; Ibid., living culture MFLUCC 11–0657. Botryosphaeria Ces. & De Not., Comm. Soc. Crittog. Ital. 1: 211 (1863) Mycobank: MB635

Possible synonyms Amerodothis Theiss. & Syd., Ann. Mycol. 13: 295 (1915) Apomella Syd., Ann. Mycol. 35: 47 (1937) Caumadothis Petr., Sydowia 24): 276 (1971) [1970] Coutinia J.V. Almeida & Sousa da Câmara, Revta agron., Lisb. 1: 392 (1903) Creomelanops Höhn., Sber. Akad. Wiss. Wien, Math.-naturw. Kl., Abt. 1 129: 146 (1920) Cryptosphaeria Ces. & De Not., Comm. Soc. Crittog. Ital. 1(4): 231 (1863) Cryptosporina Höhn., Farnesyltransferase Öst. Bot. Z. 55: 54 (1905) Desmotascus F. Stevens, Bot. Gaz. 68: 476 (1919) Epiphyma Theiss., Verh. Zool.-bot. Ges. Wien 66: 306 (1916) Fusicoccum Corda, in Sturm, Deutschl. Fl., 3 Abt. (Pilze Deutschl.) 2: 111 (1829) Polythecium Bonord., Bot. Ztg. 19: 203 (1861) Pyreniella Theiss., Verh. Zool.-bot. Ges. Wien 66: 371

(1916) Rostrosphaeria Tehon & E.Y. Daniels, Mycologia 19: 112 (1927) Thuemenia Rehm, in Thümen, Mycoth. Univ., cent.: no. 971 (in sched.) (1878) Hemibiotrophic or saprobic on leaves and wood. Ascostromata 300–500 mm diam., often erumpent through the bark, comprising a botryose aggregate, sometimes solitary, globose, brown to black, individual locules, with a central ostiole, papillate or not, cells of ascostromata having dark brown walls and arranged in a textura angularis. Peridium of locules two-layered, outer layer composed of small heavily pigmented thick-walled cells of textura angularis, inner layer composed of hyaline thin-walled cells of textura angularis. Pseudoparaphyses hyphae-like, wide, septate.

As shown in Figure 1B, dose-dependent inhibition of T24 cell proliferation by submicromolar concentrations of as -APF was specifically and significantly decreased following CKAP4 knockdown (p <.001 for comparison of CKAP siRNA-treated cells compared to both controls at concentrations

≥ 1.25 nM), indicating the importance of this receptor for mediating APF MK-1775 cell line antiproliferative activity in T24 bladder carcinoma cells. Figure 1 CKAP4 knockdown in T24 cells. A, Western blot analysis of CKAP4 protein expression in cells electroporated in the presence of no siRNA (Lanes 1 and 2), CKAP4 siRNA (Lanes 3 and 4), or scrambled non-target (NT) siRNA (Lanes 5 and 6), and treated with as -APF (APF) or its inactive control peptide (Pep). β-actin served as a standard control. B, Inhibition of3H-thymidine incorporation QNZ mouse by as -APF (APF) in cells electroporated with no siRNA, CKAP4 siRNA, or non-target siRNA. Results are shown as percent inhibition of3H-thymidine incorporation compared to control cells that did not receive as -APF treatment. Experiment was performed in triplicate twice. APF increases p53 tumor suppressor

gene expression via CKAP4 in T24 cells HPLC-purified native APF was previously shown to significantly decrease cell cycle transit and increase p53 expression in both normal human urothelial cells and T24 bladder carcinoma cells in vitro, while p53 knockdown decreased the antiproliferative effects of APF [22]. To determine whether CKAP4 mediated APF’s Compound C solubility dmso PRKACG stimulation of p53 expression, T24 cells were treated with 500 nM synthetic as- APF or its inactive peptide control and the effects on p53 mRNA and protein expression examined. As shown in Figure 2A, p53 protein expression was increased in APF-treated (as compared to control peptide-treated) nontransfected cells. Similarly, p53 protein expression was also increased in response to APF in cells transfected with non-target siRNA, whereas p53 levels changed less in response to APF following CKAP4

knockdown (Figure 2A). qRT-PCR also showed significantly increased p53 mRNA expression following APF treatment of nontransfected or non-target siRNA-transfected, but not CKAP4 siRNA-transfected, cells (Figure 2B-D) (p <.01 for both nontransfected and non-target transfected cells, and target gene mRNA relative to β-actin or GAPDH mRNA; data shown for normalization to β-actin expression, only). These findings indicate that CKAP4 also mediates the effects of APF on p53 mRNA and protein expression in T24 cells. Figure 2 p53 expression in T24 bladder cancer cells. A, Western blot analysis of p53 protein expression in cells electroporated in the presence of no siRNA (Lanes 1 and 2), CKAP4 siRNA (Lanes 3 and 4), or scrambled non-target (NT) siRNA (Lanes 5 and 6), and treated with as -APF (APF) or its inactive control peptide (Pep). β -actin served as a standard control.

Cancer Gene Ther 2000, 7:66–73.PubMedCrossRef 21. Yu YA, Shabahang S, Timiryasova TM, Zhang Q, Beltz R, Gentschev I, Goebel W, Szalay AA: Visualization of tumors and metastases in live animals with bacteria and vaccinia virus encoding light-emitting proteins. Nat Biotechnol 2004, 22:313–320.PubMedCrossRef 22. Hingorani M, Spitzweg C, Vassaux G, Newbold P005091 cost K, Melcher A, Pandha H, Vile R, Harrington K: The biology of the

sodium iodide symporter and its potential for targeted gene delivery. Curr Cancer Drug Targets 2010, 10:242–267.PubMedCrossRef 23. Lee YJ, Chung JK, Shin JH, Kang JH, Jeong JM, Lee DS, Lee MC: In vitro and in vivo properties of a human anaplastic thyroid carcinoma cell line transfected with the sodium iodide symporter gene. Thyroid 2004, 14:889–895.PubMedCrossRef 24. Cengic N, Baker CH, Schutz M, Goke B, Batimastat price Morris JC, Spitzweg C: A novel therapeutic strategy for medullary thyroid cancer based on radioiodine therapy following tissue-specific sodium iodide symporter gene expression. J Clin Endocrinol Metab 2005, 90:4457–4464.PubMedCrossRef 25. Kakinuma H, Bergert ER, Spitzweg C, Cheville JC, Lieber MM, Morris JC: Probasin promoter (ARR(2)PB)-driven, prostate-specific expression of the human sodium iodide symporter (h-NIS) for targeted radioiodine therapy of prostate cancer. Cancer

Res 2003, 63:7840–7844.PubMed 26. Scholz IV, Cengic N, Baker CH, Harrington KJ, Maletz K, Bergert ER, Vile R, Goke B, Morris JC, Spitzweg C: Radioiodine therapy of colon cancer following tissue-specific Astemizole sodium iodide symporter gene transfer. Gene Ther 2005, 12:272–280.PubMedCrossRef 27. Dwyer RM, Bergert ER, O’Connor

MK, Gendler SJ, Morris JC: In vivo radioiodide imaging and treatment of breast cancer xenografts after MUC1-SHP099 datasheet driven expression of the sodium iodide symporter. Clin Cancer Res 2005, 11:1483–1489.PubMedCrossRef Competing interests No competing financial interests exist for Kyong-Hwa Jun, Tae-Jin Song, Sepideh Gholami, Joyce Au, Dana Haddad, Carson Joshua, Chun-Hao Chen, Kelly Mojica, Pat Zanzonico, and Yuman Fong. Nanhai G. Chen, Qian Zhang, and Aladar A. Szalay are affiliated with Genelux Corporation. Authors’ contributions SG assisted with the write up of the manuscript. TS assisted in the in vivo experiments and contributed to the study design. JA contributed to the cytotoxicity assay. DH contributed to the in vivo PET and SPECT imaging. JC contributed to fluorescent imaging. CC contributed to the statistical analysis of the data. KM contributed to the viral replication assay. PZ contributed to the study design and radioactive imaging experiments. NC and QZ contributed to the viral sequence and construct. AS and YF contributed to the study design and completion of the manuscript. All authors read and approved the final manuscript.

Methods Subjects Twenty ��-Nicotinamide molecular weight male soldiers from an elite combat unit of the Israel Defense Forces (IDF) volunteered to participate in this double-blind study. Following an explanation of all procedures, risks and benefits, each participant provided his informed consent

to participate in the study. The Helsinki Committee of the IDF S3I-201 Medical Corp approved this research study. Subjects were not permitted to use any additional dietary supplementation and did not consume any androgens or any other performance enhancing drugs. Screening for performance enhancing drug use and additional supplementation was accomplished via a health questionnaire completed during participant recruitment. Participants were from the same unit, but were from three different squads. Volunteers from each squad were randomly assigned to one of two groups. The randomization procedure involved that each volunteer from the same squad to be alternatively assigned to each group. Two participants dropped from the study, one participant fractured his leg during training, while the other participant no longer wished to participate. Each participant Epigenetic Reader Domain inhibitor was from a separate group. Thus, a total of 18 participants were used in the final analysis. Using the procedures described by Gravettier and Wallnau [22]

for estimating samples sizes for repeated measures designs, a minimum sample size of n = 8 was required for each group to reach a statistical power (1-β) of 0.80 based on the jump power changes reported by Hoffman et al. [4] The first group; (BA; age 20.1 ± 0.7 years; height: 1.79 ± 0.07 m; body mass: 78.3 ± 9.7 kg) consumed 6.0 g of β-alanine per day, while the second group (PL; age 20.2 ± 1.1 years; height: 1.80 ± 0.05; body mass: 79.6 ± 7.8 kg) consumed 6 g of placebo (rice flour). During the 4-week study period all participants from all squads participated in the same advanced military training tasks that included combat skill development, physical work under ROS1 pressure, navigational training, self-defense/hand-to-hand combat and conditioning.

Testing protocol This randomized, double-blind, placebo controlled investigation was conducted at the unit’s training facilities, under the unit’s regular training protocols and safety regulations. Data collection occurred before (Pre) and after (Post) 28 days of supplementation. To create an acute fatigued state, each session required all participants to perform a 4 km run dressed in shorts, T-shirt and running shoes. Immediately following the 4 km run participants performed five countermovement jumps (CMJ). Participants then proceeded to put on their operational gear and weapon (12 kg) and ran a 120 m sprint. Following the sprint, participants proceeded as quickly as possible onto the shooting range and performed a 10-shot shooting protocol with their assault rifle.

For each OTU, there are 11 perfect-match

probes, and 11 mismatch probes, which are always analyzed in pairs. For an OTU to be considered a positive match to a probe, the signal intensity must be 1.3X the intensity of the mismatch probe [13]. The positive fraction is a measure of how many perfect-match probes matched out of the total number of probe pairs for that OTU. For this study, a positive fraction of 0.92 was used to determine the presence of an OTU in a sample; for each OTU, 92% of the perfect-match probes were positive. A mean intensity threshold of 100 was used, so that only OTUs with signal intensity greater than that were included in the analysis. All 14 sample files were used in the comparison. Data were evaluated down to the taxonomic level of family for most analyses since each OTU represented more than one species [32]. A heatmap (Figure 6) showing the presence or Buparlisib in vivo absence, and relative intensity of each OTU was created using all 14 samples. Samples were arranged in rows and were clustered on the vertical axis. OTUs were arranged vertically and were clustered on the horizontal axis.

Clustering was done using Phylotrac’s heatmap option with Pearson correlation, a measure of the correlation between two variables, and complete linkage algorithms (farthest neighbor), which clusters based on the maximum distance between two variables. Figure 6 Distribution of PhyloChip OTU’s for all 14 samples. Samples (rumen and colon) are arranged in rows and are clustered on the vertical axis (y-axis). OTU’s are arranged vertically and are on the horizontal axis (x-axis). Clustering was done for each using Phylotrac’s CB-5083 heatmap option with Pearson correlations and complete linkage algorithms. UniFrac (available from http://​bmf2.​colorado.​edu/​unifrac/​), an online statistical program, was used to analyze PhyloChip data [42, 43] and to confirm the clustering functions of PhyloTrac. Data were exported from PhyloTrac for analysis using the UniFrac statistical check details software. P-test significance was

run using all 14 environments together and 100 permutations, to determine whether each sample was significantly different from each other. A p-value of < 0.05 states that the environments were significantly clustered together. Two Jackknife environment clusters were performed using 100 Paclitaxel solubility dmso permutations, the weighted and unweighted UniFrac algorithms, and 307 minimum sequences to keep (UniFrac default for the specified conditions). Jackknife counts were provided for each node, representing the number of times out of 100 that a node was present on the tree when the tree was repeatedly rebuilt. A Jackknife percentage of >50% is considered significant. A principal component analysis (PCA) scatterplot was also created using the weighted algorithm, a chart which arranged two potentially related variables into unrelated variables on a graph, revealing underlying variance within the data. Acknowledgements The author would like to acknowledge Rachel P.