Med Chem 2004, 47:2430–2440.CrossRef 8. Kogan NM, Rabinowitz R, Levi P, Gibson P, Sandor D, Schlesinger M: Synthesis and antitumor activity of quinonoid derivatives of cannabinoids. Med Chem 2004, 47:3800–3806.CrossRef 9. Kogan NM, Blázquez C, Álvarez L, Gallily R, Schlesinger M, Guzmán M, Mechoulam R: A cannabinoid quinone inhibits angiogenesis by targeting BKM120 vascular endothelial cells. Mol Pharm 2006, 70:51–59. 10. Kogan NM, Schlesinger M, Priel E, Rabinowitz R, Berenshtein E, Chevion M, Mechoulam R: HU-331, a novel cannabinoid-based anticancer topoisomerase II inhibitor. Mol Cancer Ther 2007, 6:6173–6183.CrossRef 11. Kogan NM, Schlesinger M, Peters M, Marincheva G, Beeri R, Mechoulam R: A cannabinoid anticancer quinone,

HU-331, is more potent and less cardiotoxic than doxorubicin: a comparative in vivo study. JPET 2007, 322:646–653.CrossRef 12. Filosa R, Peduto A, De Caprariis P, Saturnino C, Festa M, Petrella A, Pau A, Pinna GA, La Colla P, Busonera B, Loddo R: Synthesis and antiproliferative properties of N3/8-disubstituted 3,8-diazabicyclo[3.2.1]octane analogues of 3,8-bis[2-(3,4,5-trimethoxyphenyl)pyridin-4-yl]methyl-piperazine. LEE011 datasheet MedChem 2007, 42:293–306. 13. Filosa R, Peduto

A, Micco SD, Caprariis P, Festa M, Petrella A, Capranico G, Bifulco G: Molecular modelling studies, synthesis and SN-38 mw biological activity of a series of novel bisnaphthalimides and their development as new DNA topoisomerase II inhibitors. MedChem 2009, 17:13–24. 14. Peduto A, Pagano B, Petronzi C, Massa A, Esposito V, Virgilio A, Paduano F, Trapasso F, Fiorito F, Florio S, Giancola G, Filosa R: Design, synthesis, biophysical and biological studies of trisubstituted naphthalimides as G-quadruplex ligands. BioorgMedChem. 2011, 21:6419–6429. 15. Petronzi C, Filosa R, Peduto A, Monti MC, Margarucci L, Massa A: Structure-based design, synthesis and preliminary anti-inflammatory activity of bolinaquinone analogues. Eur J Med Chem 2011, 46:488–496.PubMedCrossRef

16. Pengfei Z, Yanxia N, Liangqing Y, Mo C, Congjian X: The proliferation, apoptosis, invasion of endothelial-like Progesterone epithelial ovarian cancer cells induced by hypoxia. J Exp Clin Cancer Res 2010, 29:124.CrossRef 17. Deveraux QL, Reed JC: IAP family proteins–suppressors of apoptosis. Genes Dev 1999, 1:239–252.CrossRef 18. Riccardi C, Nicoletti I: Analysis of apoptosis by propidium iodide staining and flow cytometry. NatProt 2006, 1:1458–1461. 19. Caraglia M, Leardi A, Corradino S, Ciardiello F, Budillon A, Guarrasi R, Bianco AR, Tagliaferri P: Alpha-Interferon potentiates epidermal growth factor receptor-mediated effects on human epidermoid carcinoma KB cells. Int J Cancer 1995, 61:342–347.PubMedCrossRef 20. Xiao-Fen L, Cong-Xiang S, Zhong Wen Yu-Hong Q, Chao-Sheng Y, Jun-Qi W, Ping-Neng Z, Hai-Li W: PinX1 regulation of telomerase activity and apoptosis in nasopharyngeal carcinoma cells. J Exp Clin Cancer Res 2012, 31:12.CrossRef 21.

The lumen pH was measured spectroscopically through a measurement of the electrochromic shift (ECS), which is a signal arising from the Stark effect of the electric field across the thylakoid membrane on the energy levels of carotenoids embedded in the membrane (Bailleul et al. 2010; Witt 1979). This effect causes the absorption spectrum of carotenoids in the spectral region between 450 and 550 nm to shift. The extent

of spectral shift is proportional to the amplitude of the electric field and as a result can be used to measure the transmembrane electric field. The ECS measurement can be used to probe the lumen pH by shuttering off the actinic light GSK1838705A solubility dmso and measuring the “reverse ECS.” Explanations of information that can be obtained from the ECS measurement, including measurements of the lumen pH, are given in Bailleul et al. (2010), Cruz et al. (2001), and Takizawa et al. (2007). To estimate the pK as of PsbS and of qZ in vivo, Takizawa and coworkers assumed that de-epoxidized xanthophyll

(i.e., zeaxanthin or antheraxanthin) and protonated PsbS are the two components necessary for qE. This assumption involved fitting to a specific mechanistic model (Fig. 4a) and excluded the possibility that the protonation of LHC proteins is a factor in qE activation MI-503 ic50 in vivo. Nonetheless, because it followed a specific model, this assumption enabled estimates of the pH level at which qE components were activated. The pK a of PsbS activation was fitted to be 6.8, with a Hill coefficient of ∼1, and the effective pK a of qZ was fit to be 6.8 with a Hill coefficient of 4.3. This effort is one of the first attempts thus far to fit the activation levels of G protein-coupled receptor kinase qE using in vivo measurements, and the results suggest

that the pK as of PsbS and qZ are higher in vivo than the pK as for isolated glutamate (Li et al. 2002b) and for VDE in vitro (Jahns et al. 2009). Because of the challenges of estimating the lumen pH in vivo, the pK a values reported will surely be subject to refinement and reexamination. Nonetheless, the spectroscopic approach of estimating pK as and Hill coefficients is notable because the parameters are estimated from intact leaves. The approach of spectroscopically measuring the lumen pH through the ECS shift is unique and powerful in that it does not require the extraction of chloroplasts or the use of chemicals. The technique of using reverse ECS would be even more powerful it if could be extended to measure lumen pH over the course of light adaptation. Such a measurement could be used to fit mechanistic kinetic models of the protonation of the proteins involved in qE. Doing so would selleck compound provide a method for determining the pK a of qE components during the process of qE induction and would enable greater precision than steady-state measurements in measuring the pK as and Hill coefficients of qE triggering.

Receiving any type of information affected reporting more in contemplators than in precontemplators. In actioners personalized feedback Adriamycin in vivo seemed to increase the number

of notifications more than standardized feedback. find more Strong points of this study are the randomized controlled design with relatively large intervention and control groups. This minimizes potential sources of bias such as selection bias or increases in reporting due to other reporting enhancing activities like education. Another strong point is the objective measurement of the performance of physicians before and after the intervention. Actual reporting behaviour is our primary outcome measure instead of self reported change in behaviour intention. Although

changing actual reporting behaviour is the ultimate goal of our intervention, this outcome measure might have been too insensitive to evaluate the present intervention. If the intervention caused forward stage transition, moving OPs from no intention to report to considering or even planning to report, we would not know until the OP actually starts reporting. Limitations must also be considered in interpreting the results of this study. Staurosporine One of the limitations is that we did not use a staging instrument to determine the stage of reporting behaviour of participating OPs at baseline. We assumed that OPs who did not notify any occupational disease in 2006 or 2007 could be identified as immotives or precontemplators and OPs who notified before June

1st 2007 but not afterwards, could be seen as contemplators or preparators. This might be a source of misclassification because precontemplators may already have the intention to report, contemplators may have lost this intention or be actually actioners that incidentally did not have anything to report. In this study, both stage-matched PIK-5 and stage-mismatched newsletters might in fact have been addressed to more mixed behavioural groups, weakening the influence of stage-matching. On the other hand, the results show that receiving any type of information affected reporting significantly more in contemplators than in precontemplators. This indicates that OPs may differ in regard to their reporting behaviour and that they might benefit from different interventions. Another limitation of this study is that we used a single intervention in precontemplators and contemplators: a personalized newsletter was only sent once to the participants, without information on receipt, perusal and assessment of the contents. A single information intervention is likely to be inferior to a repetitive or multifaceted intervention.

SC drafted, revised the manuscript and gave final approval to the manuscript. MC helped to draft and revise the manuscript. All authors read and approved the final manuscript.”
“Background Beauveria Vuill. is a globally distributed genus of soil-borne entomopathogenic hyphomycetes that is preferred as a model system for the study of entomopathogenesis and the biological control click here of pest insects [1]. The most abundant species of the genus is Beauveria bassiana, found in

a wide host range of nearly 750 insect species, with extended studies on host-pathogen interactions at the molecular level and all the prerequisite knowledge for its commercial production [2]. B. brongniartii, the second most common species of the genus, has narrow host specificity and is well-studied as the pathogen of the European cockchafer (Melolontha melolontha), a pest in permanent grasslands and orchards [3]. Strains of both fungal species have been exploited as biological control agents (BCAs) [4, 5]. As is usually the case for most mitosporic fungi, morphological characters are inadequate for delimiting species within a genus and this website this creates a continuing demand of screening for additional taxonomic characters. Consequently, through the years, several efforts have been made to genetically characterize or differentiate Beauveria species and strains,

using various tools, including isozyme markers [6], karyotyping [7], vegetative compatibility groups [8], RAPD markers [9, 10], rRNA gene sequencing and intron analyses [11, 12], RFLPs and AFLPs [13–15], subtilisin protease genes [16], microsatellites [17, 18] and combinations of rRNA gene complex and other nuclear genes [1, 19, 20]. These approaches Carnitine palmitoyltransferase II provided valuable information on polymorphisms in populations of B. bassiana, with ITS sequences combined with other nuclear gene sequences being more reliable in taxonomic and phylogenetic studies [1, 20, 21]. Consequently,

earlier assumptions that Beauveria is strictly aBelnacasan nmr sexual have been severely hampered by the recent discoveries of Cordyceps teleomorphs associated with Beauveria [1, 22, 23]. Thus, the extent to which the entire Beauveria genus is correlated with sexual Cordyceps remains to be examined and proved [1]. Mitochondrial DNA (mtDNA), due to its properties to evolve faster than the nuclear DNA, to contain introns and mobile elements and to exhibit extensive polymorphisms, has been increasingly used to examine genetic diversity within fungal populations [24–26]. In other mitosporic entomopathogenic fungi, such as Metarhizium [27], Lecanicillium [28] and Nomurea [29], mtDNA data compared favourably to data based on ITS combined with a single nuclear gene, for applications in phylogeny, taxonomy and species or strain -identification. In Beauveria, the use of mtDNA RFLPs or partial mtDNA sequences suggested that mtDNA can be equally useful for such studies [2, 30].

B.104.6.1 Q1D006 242 7 Rhomboid Family Proteins were retrieved with GBLAST e-values between 0.1 and 0.001, individually verified and assigned TC numbers as indicated. A single protein (Q1D5P4; 432 aas; 14 TMSs) proved to be a member of the Monovalent Cation:Proton Antiporter-2 (CPA2) Family, and it was assigned TC# 2.A.37.6.1 in a novel subfamily. It could be a K+:H+ or Na+:H+ antiporter. A second protein (Q1DCP3;

290 aas; 10 TMSs) was shown to be a member of the Drug/Metabolite Transporter (DMT) Superfamily, distantly related to members of the Drug Metabolite Exporter (DME) Family. It was assigned TC # 2.A.7.31.1, also in a novel subfamily. A third protein (Q1D7B4; 506 aas; 14 TMSs) was assigned TC# 2.A.66.12.1 as a member of the Multidrug/Oligosaccharidyl-lipid/Polysaccharide (MOP) Flippase Superfamily. It belongs to a family within this superfamily for which Entinostat in vitro no functional data are available. A fourth protein (Q1DA07; 731 aas; 13 TMSs) belongs to the Major Facilitator Superfamily (MFS) and was assigned TC# 2.A.1.15.16. The gene of this protein is adjacent to a putative S-adenosyl methionine (SAM)-dependent methyltransferase

whose homologues include puromycin methyltransferases. The substrate of this protein is potentially a drug that undergoes modification by methylation for detoxification purposes. Two proteins proved to be else members of the ABC-2 Superfamily within the ATP-binding Cassette (ABC) Functional Superfamily [28]. One protein (Q1D520; 1200 P-gp inhibitor aas; 13 TMSs) was assigned to a new ABC family with TC# 3.A.1.145.1. Notably, this exporter proved to be a fusion between an N-terminal ABC-2 domain with 13 putative TMSs and a hydrophilic C-terminal zinc dependent amino peptidase domain (Peptidase M1 Family), suggesting that the transporter domain

could be involved in the export of an amino acid, amino acid derivative, or product of amino acid metabolism. In addition, Q1D520 resembles (35.4% identity and 54.6% similarity with 4 gaps) 3.A.1.145.3, another ABC-2 export permease fusion protein annotated as being involved in multi-copper enzyme maturation. The other ABC protein (Q1D0V1; 266 aas; 6 TMSs) was assigned TC# 3.A.1.144.3 and is functionally uncharacterized. Two proteins were shown to be homologous to proteins in TC Category 9. The first protein (Q1CXZ2; 211 aas; 3 TMSs) was found to be a member of the Protein Tyrosine Kinase inhibitor Cannabalism Toxin SdpC (SdpC) Family and was assigned TC# 9.B.139.2.1. The second protein (Q1D006; 242 aas; 7 TMSs) was assigned TC# 9.B.104.6.1. It belongs to the Rhomboid Protease Family and shows sequence similarity to members of the MFS; this result provides preliminary evidence that the MFS and Rhomboid Protease Family may in fact be homologous and warrants future investigation.

Results Significant group × time interaction effects (p ≤ .05) were observed with BIOCREAT and creatine groups compared to placebo in changes of lean mass (PL: .4 ± 1.7 kg, CRE: 1.8 ± 2.1 kg, BIO: 1.8 ± 1.3 kg) and bench press 1 RM (PL: 8 ± 10.7 lbs, CRE: 21 ± 13 lbs, BIO: 16 ± 11 lbs). Further analysis revealed that the BIO group had a significantly (p ≤ .05) greater Wingate peak power (PL: 18.9 ± 55.7 watts, CRE: 12.1 ± 70.4 watts, BIO: 55.8 ± 66.1 watts) at the four week time point in comparison to PL and CRE. Significant main effects for time (p ≤ .05) were observed on body weight, fat mass, body fat percentage, leg press, and Wingate mean

power. No significant interactions were observed among groups for muscular endurance on bench press or leg press or in any clinical safety data including lipid panel, liver function, kidney function, and/or Bcl-2 inhibitor CBC panel (p > 0.05). Conclusion It is concluded that BIOCREAT supplementation JPH203 chemical structure had a significant impact on upper body strength and body composition in comparison to placebo in a double blind controlled trial. The results obtained also demonstrated that there was no significant difference between

BIOCREAT and the dextrose/creatine mixture on parameters of upper body strength and body composition. These changes were obtained with no clinical side effects. We conclude that in addition to a structured resistance training program, BIOCREAT can significantly increase strength and muscle mass. Acknowledgements This Study was sponsored by INDUS BIOTECH.”
“Background BCAAs (leucine, isoleucine, and valine), particularly leucine, activate key enzymes in protein synthesis after physical exercise. Research has demonstrated that BCAAs increase mTOR phosphorylation and activate p70 S6 kinase in human muscle via an Cytidine deaminase Akt-independent

pathway. The extent to which BCAAs influence the anabolic hormone response in conjunction with resistance exercise is not well established. A randomized, double-blind, placebo-controlled study was performed to evaluate the effects of BCAA ingestion in conjunction with an acute bout of lower-body resistance exercise (RE) on various anabolic hormones. Methods 20 recreationally active males ingested a BCAA supplement (120 mg/kg/bw) (n = 10; 24.4 years; 178.3 cm; 85.4 kg) or a placebo (n = 10; 21 years; 176.8 cm; 83 kg) at 3 time points: 30 minutes prior to RE, and immediately pre-RE and immediately post-RE. Subjects performed 4 sets of leg press and 4 sets of leg extension at 80% 1 RM to failure. Rest periods between sets and exercises was approximately 150 seconds. Venous blood was sampled at baseline; 30 min later, immediate Volasertib purchase postexercise, 30 min post-exercise; 2 hrs post-exercise, and 6 hrs post-exercise for serum insulin, growth hormone (GH), and free insulin-like growth factor-1 (IGF-1). A two-way ANOVA with repeated measures was utilized to analyze the data.

Small 2006,2(6):747–751.CrossRef 29. Yu WW, Qu L, Guo W, Peng X: Experimental determination of the extinction coefficient of CdTe, CdSe, and CdS nanocrystals. Chem Mater 2003,15(14):2854–2860.CrossRef 30. Alivisatos AP: Semiconductor clusters, nanocrystals, and quantum dots. Science 1996,271(5251):933–937.CrossRef 31. Li YX, Yang P, Wang P, Huang X, Wang L: CdS nanocrystal induced chemiluminescence: reaction mechanism and applications. Nanotechnology 2007,18(22):225602.CrossRef 32. Hua LJ, Han HY, Zhang XJ: Size-dependent electrochemiluminescence behavior of water-soluble CdTe quantum dots

and selective sensing of L -cysteine. Talanta 2009,77(5):1654–1659.CrossRef 33. Chen H, Gao F, He R, Cui D: Chemiluminescence of luminol catalyzed by silver nanoparticles. J CRT0066101 Colloid Interface Sci 2007, 315:158–163.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions BL, JB, and HD carried out the experimental work, participated in the planning of the experiment and drafted the manuscript. ZP and LD participated

in the argument on this manuscript and the manuscript was touched up by them. All authors read Z-DEVD-FMK supplier and approved the final manuscript.”
“Background The collective absorption (emission) of photons by an ensemble of identical atoms ‘provides valuable insights into the many-body physics of photons and atoms’ (quoted from [1]). Taking into selleck chemicals account the

quantization of electromagnetic field, many fundamental and interesting properties of the coupled systems of atoms and field are revealed. For example, when the average distances between atoms are much less than the ‘resonant transition’ wavelength of emitted (absorbed) light, the cooperative coupling leads to a substantial radiative shift of the transition energy and significant change in decay rate of the ensemble state. The latter was revealed through the various P-type ATPase theoretical (for example, some relatively modern researches in [2–5]) and experimental investigations (see starting, for example, from [6, 7] to the modern applications like described in [8] and impressively effective experimental realizations as in [1]). Some peculiar behavior in spontaneous emission is proper even in a system of atoms which can have a relative distance larger than the emission wavelength (see, for instance, [9]), and initially, only one atom or one-photon state is excited, as discovered in this paper. In the present paper, a system (chain) of N identical two-level non-interacting atoms, prepared ‘via a single-photon Fock state’ in the one- or two-mode resonator, is investigated. The main goal of the paper is to obtain the information about the state of electromagnetic field and atomic system (chain) in a Weisskopf-Wigner approximation (see [10] chapter 6, page 206 and some comments in [11]).

pecorum lineage may require a rigorous MLST approach that incorporates genetic data from several more independent loci and extensive geographic sampling. It is clear that the ompA gene is distorted by technical and biological interference rendering it incapable of representing find more true phylogenetic divisions as a molecular marker, yet it remains useful as a fine-detailed, cost-effective, comparative marker for fine-detailed epidemiological investigation of large numbers of koala C. pecorum positive samples. Alternatively, the tarP gene’s

ability as a “”neutral marker”" to provide a “”bird’s-eye-view”" on higher levels of evolutionary divergence between koala populations and ORF663′s opportunities as a contingency marker are promising for future phylogenetic studies in the koala. While three out of our four shortlisted genes (including ompA) proved to be effective gene markers, incA was ultimately deemed to be the least effective and was discarded from further analysis. However, the significant discrepancy noted between the mean diversity of incA from koala and non-koala hosts (as well FHPI as ORF663) invites intriguing questions regarding the genetic diversity of C. pecorum beyond the koala host which, while outside the scope of this

study, will be important in subsequent see more research in this area. Although this study focussed on a mere 10 genes in the C. pecorum genome, it successfully challenged ompA as a molecular marker and provided an important opportunity to review previous knowledge on the genetic diversity of C. pecorum in Australian koala populations. The availability of the complete E58 C. pecorum genome sequence and, eventually, a koala C. pecorum genome, will facilitate the characterisation of additional genes and promote further analyses of genomic variation to support comprehensive surveys of lineage prevalence within and between koala populations. Until then, the data described here provides a solid foundation for this subsequent research by highlighting a robust measurement tool for koala C. pecorum infections and presents a compelling depiction

of their phylogenetic relationships. This application will have importance for our ability to successfully map, control and manage diseased populations of this dwindling native icon. Acknowledgements Farnesyltransferase The authors would like to acknowledge the generosity of Gary Myers, Institute for Genome Sciences, University of Maryland, Baltimore, USA for allowing us access to the C. pecorum E58 genome sequence. We would also like to acknowledge Jon Hanger and Jo Loader (Australian Wildlife Hospital, Beerwah, Australia), Jon Callaghan (Gold Coast City Council, Gold Coast, Australia) and Jeff McKee (Ecosure, Gold Coast, Australia) for their valuable contribution to the collection of koala swabs from Brendale, Narangba, East Coomera and Pine Creek koala populations, respectively.

28–7.34 (m, 1H, Harom), 7.41–7.47 (m, 1H, Harom),7.52–7.59 (m, 1H, Harom), 7.92–7.99 (m, 2H, Harom), 8.06–8.11 (m, 1H, H-1), 8.44 (s, 1H, H-6); EI-MS m/z: 362 (M+, 100 %); Anal. calcd. for C21H22N4S: C, 69.58; H, 6.12; N, 15.46; S, 8.84. Found: C, 69.54; H, 6.07; N, 15.40; S, 8.82. 12-(3-(N,N-dimethylamino)propyl)-12(H)-pyrido[2,4-e]quino[3,4-b][1,4]thiazine (7e) Yield 58 %; an oil;

1H NMR (CDCl3, 500 MHz) δ (ppm): 1.63–1.78 (m, 2H, CH2 CH 2CH2), 1,98 (s, 6H, N(CH3)2), 2.18–2.24 (t, J = 7.2 Hz, 2H, (CH3)2NCH 2), 4.01–4.12 Gamma-secretase inhibitor (t, J = 7.3 Hz, 2H, NCH2), 7.04–7.11 (m, 1H, H-11), 7.28–7.36 (m, 1H, Harom),7.41–7.48 (m, 1H, Harom), 7.53–7.61 (m, 1H, Harom), 7.98-8.01 (m, 2H, Harom), 8.08–8.14 (m, 1H, H-1), 8.46 (s, 1H, H-6); EI-MS m/z: 336 (M+, 100 %); Anal. calcd. for C19H20N4S: C, 67.83; H, 5.99; N, 16.65; S, 9.53. Found: C, 67.74; H, 5.93; N, 16.61; S, 9.50. Antiproliferative assay in vitro Cell culture The synthesized compounds were evaluated for their anticancer activity using two cultured cell lines: SNB-19 (human glioblastoma, DSMZ – German Collection of Microorganisms and Cell Cultures, GSK2879552 clinical trial Braunschweig, Germany) and C 32 (human amelanotic melanoma, ATCC—American Type Culture Collection,

Rockville, MD, USA). The cultured cells were kept at 37 °C and 5 % CO2. The cells were seeded (1 × 104 cells/well/100 μl D-MEM supplemented with 12 % FCS and streptomycin and penicillin) using 96-well plates (Corning). WST-1 assay Antiproliferative effect of compounds 4 and 7 was determined using

the Cell Compound Library supplier Proliferation Reagent WST-1 assay (Roche Diagnostics, Mannheim, Germany). This colorimetric assay is based on the cleavage of the tetrazolium salt WST-1 by mitochondrial dehydrogenases in viable cells, Quinapyramine leading to formazan formation. After exposure to tested compounds (at concentrations between 0 and 100 μg/ml) for 72 h, cells were incubated with WST-1 (10 μl) for 2 h, and the absorbance of the samples against a background control was read at 450 nm using a microplate reader. Results are expressed as means of at least two independent experiments performed in triplicate. Acknowledgments The study is supported by the Medical University of Silesia (Grant KNW-1-073/P/1/0). Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. References Amaral L, Kristiansen JE (2000) Phenothiazines: an alternative to conventional therapy for the initial management of suspected multi-drug resistant tuberculosis. Int J Antimicrob Agents 14:173–176PubMedCrossRef Bansode TN, Shelke JV, Dongre VG (2009) Synthesis and antimicrobial activity of some new N-acyl substituted phenothiazines. Eur J Med Chem 44:5094–5098PubMedCrossRef Clarke FH, Silverman GB, Wotnick CM, Sperber N (1961) 3-Azaphenothiazine and dialkylaminoalkyl derivatives.

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