The elution profile of this column (Figure 3) was monitored by as

The elution profile of this column (Figure 3) was monitored by assaying aliquots of each column fraction with ChromeAzurol reagents according to the protocol previously developed by McPhail et al.[12]. The profile exhibited a distinct peak of Cu-binding activity (expected to correspond to {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| compounds containing amino groups) followed by a smaller peak, both of which overlapped an extended peak of Fe-binding activity (reflecting the elution of contaminating phosphate from the culture medium). The fractions corresponding

to the larger peak of Cu-binding activity were pooled, taken to dryness in vacuo, and the recovered solids dissolved in 76% ethanol for preparative TLC fractionation. Following preparative TLC, the area on the TLC plate corresponding to the position of the ninhydrin-reactive compound was scraped from each plate and extracted with deionized Selleckchem Metabolism inhibitor Temsirolimus mouse water. The combined aqueous extracts were dried in vacuo and dissolved in a small volume of deionized water for rechromatography

on a Sephadex G-15 column. Figure 3 Initial Sephadex G-15 column fractionation of an 85% ethanol extract of dried culture filtrate from Pseudomonas fluorescens SBW25. The solids from 840 mL of dried SBW25 culture filtrate were extracted with 85% ethanol as described in the Methods section. A portion of the extract equivalent to 800 mL of original culture filtrate was taken to dryness in vacuo and dissolved in 6 mL of deionized water for application to a Sephadex G-15 column equilibrated in the same solvent. The column was eluted with deionized water. Fractions (6 mL each) were collected and analyzed for ADAMTS5 reaction with the Fe- and Cu-CAS reagents as described in the Methods section. The fractions corresponding to the largest Cu-binding

peak were pooled (as indicated by the double arrow) for concentration and further purification by preparative TLC fractionation. The elution profile for Sephadex G-15 column fractionation of the material recovered from preparative TLC purification exhibited a Cu-binding peak that was clearly separated from a smaller Fe-binding peak, indicating that the ninhydrin-reactive compound was separated from the contaminating phosphate (Figure 4). The fractions from the Cu-binding peak were pooled as indicated, and an aliquot of this pooled material was tested for antimicrobial activity in agar diffusion assays. The tested aliquot strongly inhibited the growth of D. dadantii 1447. The pooled fraction was then taken to dryness and re-dissolved in 76% ethanol. TLC analysis of an aliquot of the 76% solution gave a single ninhydrin-staining band at the expected Rf, and no UV-absorbing or fluorescent compounds were detected. The remainder of the 76% ethanol solution of the purified compound, corresponding to ca. 600 mL of original culture filtrate, was concentrated in vacuo and yielded 3.7 mg of a white amorphous solid, of which 3.

Mature form of adrenomedullin is a useful marker to evaluate bloo

Mature form of adrenomedullin is a useful marker to evaluate blood volume in hemodialysis patients. Am J Kidney Dis. 2002;40:794–801.PubMedCrossRef 15. Shimosawa T, Kanozawa K, Nagasawa R, Mitarai T, Isoda K, Takahashi K, et al. Adrenomedullin amidation enzyme activities in hypertensive patients. Hypertens Res. 2000;23:167–71.PubMedCrossRef 16. Mizutani M, Ito

Y, Mizuno M, Nishimura H, Suzuki Y, Hattori R, et al. Connective tissue growth factor (CTGF/CCN2) is increased in peritoneal dialysis patients with high peritoneal solute transport rate. Am J Physiol Renal Physiol. 2010;298:F721–33.PubMedCrossRef”
“Introduction Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease characterized by the progressive enlargement of

innumerable renal cysts that lead to the deterioration of kidney function [1–3]. The Consortium for Radiologic Imaging Studies of Polycystic Kidney Disease (CRISP) study showed that baseline Ferrostatin-1 manufacturer total kidney PF-01367338 in vitro volume (TKV) predicted the subsequent rate of an increase in volume, independently of age [4]. Higher rates of kidney enlargement are associated with a more rapid decrease in renal function. In a more recent study on CRISP participants, height-adjusted TKV (ht-TKV) predicted the risk of developing renal insufficiency in ADPKD patients within 8 years of follow-up [5]. The reason for adopting ht-TKV as an adjusted TKV marker in this study was to minimize the differences in adjusted TKV values between men and women. Other adjusted TKV markers, such as body surface-adjusted TKV (bs-TKV) or log-converted TKV (log-TKV), were compared from the standpoint of minimizing the differences between men and women. It remains unclear which adjusted TKV marker correlates best with renal

function. On the other hand, the results from three recent prospective clinical trials examining the effect of mammalian target of rapamycin over inhibitors on disease progression of ADPKD have not demonstrated an association between changes in TKV and glomerular filtration rate (GFR) [6–8]. These studies might have used too short a period for examining the relationship between TKV and functional changes. If TKV correlates with kidney function, it will be a useful clinical marker of renal function since (1) it can be measured reliably, and (2) it changes by a see more measurable amount during a relatively short period of time (mean % increase of TKV is 5–6 % per year) [9]. In contrast, kidney function, measured by estimated GFR (eGFR), decreases at a slow rate of 0–3 ml/min/1.73 m2 per year depending on the chronic kidney disease (CKD) stage [10]. Taking the measurement variation of eGFR into consideration, it is difficult to detect a small change as significant, especially during early CKD stages when a relatively small amount of eGFR decreases from a relatively large baseline eGFR. For the above reasons, we reappraised the relationship between kidney volume and kidney function (using eGFR).

Parasitol Res 2004, 92:113–120 PubMedCrossRef 25 TriTryp DB: Kin

Parasitol Res 2004, 92:113–120.PubMedCrossRef 25. TriTryp DB: Kinetoplastid genomic resources Database. [http://​triTrypdb.​org/​common/​downloads/​release-4.​1/​Tcruzi/​fasta/​TriTrypDB]

[] 26. Aslett M, Aurrecoechea C, Berriman M, Brestelli J, Brunk BP, Carrington M, Depledge DP, Fischer S, Gajria B, Gao X, Gardner MJ, Gingle A, Grant G, Harb OS, Heiges M, Hertz-Fowler C, Houston R, Innamorato F, Iodice J, Kissinger JC, Kraemer E, Li W, Logan FJ, Miller JA, Mitra S, Myler PJ, Nayak V, Pennington C, Phan I, Pinney DF: TriTrypDB: a functional genomic resource for the Trypanosomatidae. Nucleic Acids Res 2010, 38:457–462.CrossRef 27. Larkin MA, Blackshields G, Brown NP, Chenna R, McGettigan PA, McWilliam H, Valentin F, Wallace IM, Wilm A, Lopez R, Thompson JD, Gibson WH-4-023 in vitro TJ, Higgins DG: Clustal W and Clustal X version 20. Bioinformatics 2007, 23:2947–2948.PubMedCrossRef 28. Gouy M, Guindon S, Gascuel O: SeaView version 4: A multiplatform graphical user interface for sequence alignment and phylogenetic tree

building. Mol Biol Evol 2010, 27:221–224.PubMedCrossRef 29. Crooks GE, Hon G, Chandonia JM, Brenner SE: WebLogo: a sequence logo generator. Autophagy Compound Library Genome Res 2004, 14:1188–1190.PubMedCrossRef 30. Hirokawa T, Boon-Chieng S, Mitaku S: SOSUI: classification and secondary structure prediction system for membrane proteins. Bioinformatics 1998, 14:378–379.PubMedCrossRef 31. Bendtsen JD, Nielsen H, von Heijne G, Brunak S: Improved prediction of signal peptides: SignalP 30. J Mol Biol 2004, 340:783–795.PubMedCrossRef 32. Zingales B, Andrade SG, Briones MR, Campbell DA, Chiari E, Fernandes O, Guhl F, Lages-Silva E, Macedo AM, Machado CR, Miles MA, Romanha AJ, Sturm NR, Tibayrenc M, Schijman AG: A new consensus for this website Trypanosoma cruzi intraspecific nomenclature: second revision meeting recommends TcI to TcVI. Mem Inst Oswaldo Cruz 2009, 104:1051–1054.PubMedCrossRef

STK38 33. Cano MI, Gruber A, Vazquez M, Cortés A, Levin MJ, Gonzalez A, Degrave W, Rondinelli E, Ramirez JL, Alonso C, Requena JM, Franco Da Silveira J: Molecular karyotype of clone CL Brener chosen for the Trypanosoma cruzi genome project. Mol Biochem Parasitol 1995, 7:273–278.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MMK-M, LL and WDR carried out the molecular genetic studies, microscopy analyses, sequence alignments and phylogenetic analyses. RMCP and PRA participated in molecular genetic studies. RPM-Neto and DCB participated in the sequence and phylogenetic analyses. RAM participated in the microscopy analyses. WDR and SMRT designed and coordinated the study and drafted the manuscript. All authors have read and approved the final manuscript.

Photoperiod was 12 h with 350 μmol m−2 s−1 PPFD and temperature w

Photoperiod was 12 h with 350 μmol m−2 s−1 PPFD and temperature was cycled 23/20 °C (light/dark). Instantaneous whole-canopy gas exchange rate was measured using a LI-6400 (Li-Cor Inc., Lincoln, NE, USA) with a custom-made whole-shoot Arabidopsis cuvette (Fig. 1). Cuvette PPFD was maintained at 350 μmol m−2 s−1

PPFD, CO2 was maintained at 400 μmol mol−1, and temperature and relative humidity were set to growth chamber conditions. Each block was measured on a XAV-939 mouse different day, 28–31 days after sowing. Following measurements for each plant, leaf area was determined from digital photographs of the rosette using Scion Image (Scion Corporation, Frederick, MD, USA). Fig. 1 Cuvette used for whole-plant gas exchange measurements. The cuvette is mounted on the LI-6400 IRGA and cuvette control system (gold-plated panel, fan and aluminum box, upper photograph). This system allows accurate, rapid measurement of CO2 (A) and H2O (E) exchange of whole shoots of Arabidopsis plants. The whole-plant cuvette incorporates a leaf temperature thermocouple that interfaces directly with the LI-6400. Intrinsic WUE (A/g s), stomatal conductance (g s), internal CO2 concentration (C i), and other variables can be calculated from

these measurements. All interior surfaces are Teflon coated or Ni-plated, the cuvette has extremely Z-IETD-FMK nmr low leak rates when operated in lab conditions with high external CO2, and the circular design provides excellent mixing using the LI-6400 fans. Plants can be rapidly changed using multiple inserts (lower photo) A:C i responses were measured for three accessions (Tsu-1, SQ-8, and Kas-1) which differed in A and δ13C. Cuvette conditions were the same as above, old but light was increased to

1,000 μmol m−2 s−1 PPFD. Photosynthetic carbon dioxide response curves were measured on four rosettes of each accession. The number of replications of A:C i measurements were limited by chamber environment equilibration time at each CO2 set point. The least squares iterative curve-fitting procedure (Sharkey et al. 2007) model was used to fit Farquhar et al.’s (1980) biochemical model of photosynthesis and obtain maximal carboxylation rate (V cmax) and maximal photosynthetic electron transport rate (Jmax). Leaf water content (Experiment 3) 39 natural accessions from the native range of Arabidopsis previously used in Mckay et al. (2003) were measured for LWC and leaf δ13C. Four replicates of each ecotype were grown in a greenhouse at UC Davis in a randomized block design. Seeds were sown in 250-mL pots in peat-based potting mix with slow-release fertilizer and vernalized at 4 °C for 5 days. Day length was extended to 16 h using supplemental lighting at 350 μmol m−2 s−1 PPFD. Greenhouse mean relative humidity and air temperature were 44 % and 23 °C, respectively.

Bentzen et al reported enhanced RT-induced pulmonary fibrosis in

Bentzen et al. reported enhanced RT-induced pulmonary fibrosis in patients treated with concomitant tamoxifen [29]. This effect was not observed in our MK-0457 supplier cohort of patients. In accordance with Wennemberg et al. [25] no correlation was found between HU and either chemotherapy or TAM. Nevertherless the very low incidence

learn more of lung toxicity was certainly also related, in our series, to the very low values of doses administered to the lung volume as shown from the calculated dose volume histograms. Statistically significant changes in toxicity ≥G2 and ≥G1 based on DLCO (p = 0.006 and p = 0.034, respectively) were detected when comparing data of patients who did receive chemo-therapy and those who did not, but no adjunctive effects were seen due to radiotherapy. These findings are in accordance with the low observed mean DLCO caused by the adjuvant chemotherapy [27, 30]. This confirms that DLCO is a more sensitive variable of functional pulmonary changes due to drug-induced toxicity. These differences were lost at BVD-523 cell line 2 years post-radiotherapy indicating recovery over time and no additional influence of hypo-fractionated radiotherapy schedule. These results confirm the literature [27], indicating a trend towards normalization at 5 months after radiotherapy. FEV1% showed a significant correlation

with smoking habits for ≥G1 toxicity at 2-years post-radiotherapy. Our findings support the hypothesis that this new hypofractionated schedule neither implies a detriment of functional breathing nor hinders Florfenicol the recovery over time. Conclusion The radiotherapy schedule investigated in this study (i.e 34 Gy in 3.4 Gy/fr plus boost dose of 8 Gy in single fraction) is a feasible and safe treatment and does not lead to adjunctive acute and late toxicities. A longer follow up is expected to confirm these favourable results. Still, randomized prospective studies, designed to validate accelerated hypofractionated schedules, should be encouraged. References 1. Veronesi U, Marubini E, Mariani L, Galimberti V, Luini A, Veronesi P, Salvadori B, Zucali R: Radiotherapy after breast-conserving

surgery in small breast carcinoma. Long-term results of a randomized trial. Ann Oncol 2000, 12:997–1003.CrossRef 2. Fisher B, Anderson S, Bryant J, Margolese RG, Deutsch M, Fisher ER, Jeong JH, Wolmark N: Twenty-year follow-up of a randomized trial comparing total mastectomy, lumpectomy and lumpectomy plus irradiation for the treatment of invasive breast cancer. N Engl J Med 2002, 347:1233–1241.PubMedCrossRef 3. Early Breast Cancer Trialist’s Collaborative Group: Effects of radiotherapy and of differences in the extent of surgery for early breast cancer on local recurrence and 15-year survival: an overview of the randomised trials. Lancet 2005, 366:2087–2106. 4. Fowler JF: The linear-quadratic formula and progress in fractionated radiotherapy.

For instance, as for EA data, the oxygen content of the carbons i

For instance, as for EA data, the oxygen content of the carbons increased from 17.6 to 36.7 wt% and 41.5 wt% after oxidizing selleck chemical pristine CDC by HNO3 at 50°C and 80°C, respectively. The subsequent H2 reduction decreased the oxygen contents to 11.2 and 20.5 wt% for CDC-50 and CDC-80, respectively. Table 1 Specific surface areas, pore structure parameters, and oxygen contents of CDCs Sample S BET a V micro b V total c Pore sized O content (m2 g−1) (cm3 g−1) (cm3 g−1) (nm) EA (wt%) XPS (wt%) EDS (wt%) Pristine CDC 1,216 0.59 0.65 2.13 17.6 8.7 6.8 CDC-50 907 0.43 0.47 2.06 36.7 14.6

20.3 CDC-50-HR 1,115 check details 0.51 0.58 2.08 11.2 10.2 10.3 CDC-80 449 0.22 0.24 2.15 41.5 15.7 29.8 CDC-80-HR 497 0.22 0.27 2.21 20.5 14.2 16.0 aBET specific surface area. bMicropore volumes calculated by the t-plot method. cSingle-point total pore volume measured at p/p 0 = 0.995. dPore size = 4V total/S BET. Nitrogen physisorption measurements were performed at selleck kinase inhibitor 77 K to characterize the surface areas and pore structures of CDCs. The N2 adsorption isotherms of all the carbons (Additional file 1: Figure S2) exhibit type I isotherms, and no hysteresis loop can be observed for these samples, indicating the microporous nature of these carbons and the absence of mesopores. The detailed specific surface area and pore structure parameters

of these carbons are listed in Table 1. The specific surface area PLEK2 and micropore volume decrease from 1,216 m2/g and 0.59 cm3/g to 907 m2/g and 0.43 cm3/g, respectively, after

oxidizing the pristine CDC by HNO3 at 50°C, which is due to the introduction of oxygen-containing groups to the pore surface of the carbon. After H2 reduction, the specific surface area and micropore volume increase back to 1,115 m2/g and 0.51 cm3/g, indicating that the oxygen-containing groups are effectively removed from the pore surface by H2 reduction. This result coincides with the elemental analyses data. It is also suggested that the oxidation of the pristine CDC by HNO3 at 50°C did not obviously damage the pore structure of the carbon and that the decrement in the specific surface area and micropore volume due to the oxidation can be mostly recovered by H2 reduction. By contrast, oxidizing the pristine CDC by HNO3 at 80°C results in the dramatic decrease of the specific surface area and micropore volume. Although the subsequent H2 reduction can effectively remove oxygen-containing groups from CDC-80, the surface area and micropore volume cannot be recovered, indicating that HNO3 oxidation at 80°C severely damaged the micropore structure of the carbon. In order to further clarify the pore structure evolution caused by HNO3 oxidation, TEM observations were also conducted to get the microscopic morphology of the CDC.

However, CL depletion had no effect on susceptibility to the anti

However, CL depletion had no effect on susceptibility to the antimicrobial peptides ASABF-α and nisin. It is possible that the net negative charge is compensated for by other membrane components such as mTOR inhibitor PG. In fact, the PG level was increased in the mutants that did not

accumulate CL. The importance of positively MM-102 charged lysyl-phosphatidylglycerol (LPG) (or MprF protein) in resistance to cationic antimicrobial peptides has been reported [43, 44], and the LPG level was not different between wild-type S. aureus and cls mutants. In addition to the probable effect of cell surface charge, we have previously reported that cell wall thickness is an important factor affecting resistance to the antimicrobial peptide ASABF-α [33]. Furthermore, in the present study, ASABF-α-resistant strains had cell walls that interfered with CL extraction (Additional file 1, Figure S1). Cell wall thickness may also be related to resistance

against other antimicrobial peptides in S. aureus [45, 46]. Our data indicate that lysostaphin treatment is critical for the efficient extraction of CL from S. aureus. Previous reports have suggested that CL is not readily extractable from B. subtilis and other Gram-positive bacteria without lysozyme treatment [47]. This may be attributable to its large molecular mass (~1500 Da) relative to that of other phospholipids, owing to its four acyl residues. However, ~25-kDa globular hydrophilic molecules can pass freely through the ~2-nm holes in the peptidoglycan polymer that forms the cell wall of Gram-positive bacteria [48]. Instead, the efficiency Epacadostat concentration Meloxicam of CL extraction is likely reduced by its physical interactions with cell wall components; for example, when CL is bound to cell wall components, it will not efficiently enter the organic phase during extraction. The membrane of the L-form variants of S. aureus is thought to express certain features that support cell growth and survival in the absence of a rigid cell wall. One study reported that a particular L-form strain had an increased CL level [36].

Our data demonstrate that the cls2 gene is important for normal L-form generation. However, the cls1/cls2 double mutant still produced L-form cells, suggesting the existence of a CL-independent mechanism. Thus, multiple mechanisms may function in cooperation to generate L-form variants. The production of a number of factors such as carotenoids, catalase, coagulase, lipase, fibrinolysin, hemolysin, and enterotoxin changes upon L-form generation and reversion [49–52]. However, none of these represents a common L-form variant phenotype, suggesting that L-form generation is associated with a drastic phenotypic conversion. The increase in CL content may be important, but not essential, for membrane stabilization. In this study, both cls1 and cls2 were shown to encode functional CL synthases.

suis, C felis, C psittaci, C caviae, and C pecorum [3–5] For

suis, C. felis, C. psittaci, C. caviae, and C. pecorum [3–5]. For the purpose of this research paper, we will refer to koala C. pecorum strains using this proposed nomenclature. While each

of these are responsible for a number of disease states in a wide range of animals (including humans), the prevalence and transmission this website of C. pneumoniae and C. pecorum throughout Australian koala populations has contributed to a significant decline in koala numbers and remain a critical threat to the koala’s continued survival [6–8]. C. pneumoniae and C. pecorum have been isolated from most koala populations investigated, with C. pecorum found to be the most widespread and pathogenic of the two species [7–10]. Notably, C. pecorum is also recognised as a pathogen and causative agent of polyarthritis and abortion in sheep and Androgen Receptor phosphorylation cattle [11]. In the koala, clinical manifestations of C. pecorum include ocular infection

leading to conjunctival scarring and blindness, respiratory tract infection, urinary tract infection causing incontinence, and genital tract infection potentially leading to infertility [6, 7, 12–14]. The latter disease signs have been implicated in lowered reproductive rates in wild koala populations in several parts of Australia, highlighting the need to understand this complex host-parasite relationship for the purpose of effective management and control strategies [8]. Questions remain about the evolutionary origin of C. pecorum in koalas, given its traditional role as a pathogen of sheep and cattle, and the modes of transmission within and between geographically isolated koala populations. In an attempt to understand these questions, Metabolism inhibitor Jackson et al., have previously BCKDHA performed fine-detailed epidemiological surveys of C. pecorum-infected koala populations, revealing that C. pecorum is genetically very diverse [7]. This analysis was performed on short variable domain IV (VDIV)

sequence fragments of the ompA gene, encoding the surface-exposed major outer membrane protein (MOMP) which is common to all members of the Chlamydiaceae [15]. There are currently eight ompA VDIV genotypes that have been identified, following several studies of geographically isolated koala populations in Australia [7, 8, 14, 16, 17]. While the majority of these genotypes are apparently confined to the koala host, several identical or near-identical sequences have been found in European sheep and cattle implying the possibility of cross-species transmission events between these hosts [7]. Questions, however, remain regarding the use of ompA as a single gene marker of chlamydial diversity. From a phylogenetic perspective, previous studies in other chlamydial species have demonstrated that ompA phylogenies are not congruent with the phylogeny of other gene targets, including other membrane proteins [18–20]. Similar observations have also been made for non-koala strains of C. pecorum [11, 21], indicating that C.

Am J Surg 2003, 185:194–197 PubMedCrossRef 23 Peña BM, Taylor GA

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“The first order of business must be to thank the previous editors of the CoFT, Dorothy Becvar (2007–2011), Bill Nichols (1987–2007) and Gerald Zuk (founding editor, 1979–1985) who are truly the giants whose shoulders we will stand upon. It is a massive task to found, develop, and maintain a journal that is not financially or intellectually supported by a large professional organization for nearly 35 years. In addition, it is important to recognize the role of our publisher Springer (http://​www.​springer.