App Env Microbio 2003, 69:5543–5554.CrossRef 20. Wanner G, Formanek H: A new chromosome model. J Struct Biol 2000, 2:147–161.CrossRef 21. Wang J, Hitchcock AP, Karunakaran C, Prange A, Franz B, Harkness T, Lu Y, Obst M, Hormes J: 3D chemical and elemental imaging by STXM spectro-tomography,

XRM2010. AIP Conf Proc 2010, 1365:215–218. Competing interests The authors declare that they have no competing interests. AZD2281 in vivo Authors’ contributions The manuscript was written through contributions of all authors. All authors have given approval to the final version of the manuscript.”
“Background Global warming caused by large-scale emission of carbon dioxide (CO2) in the atmosphere and the depletion of fossil fuels are two critical issues to be addressed in the near future [1].

Great effort has been made to reduce CO2 emissions. Technologies involving carbon capture and geological sequestration have accelerated in R788 the past decade [2]. Unfortunately, most of the associated processes require extraneous energy input, which may result in the net growth of CO2 emission. Furthermore, there are many uncertainties with the long-term underground storage of CO2. In this regard, the photocatalytic reduction of CO2 to produce hydrocarbon fuels such as methane (CH4) is deemed as an attractive and viable approach in reducing CO2 emissions and resolving the energy crisis [3, 4]. Many types of semiconductor photocatalysts, such as TiO2[5], ZrO2[6], CdS [7], and combinations thereof [8] have been widely studied for this purpose. By far the most researched photocatalytic material Cell press is anatase TiO2 because of its long-term thermodynamic stability,

strong oxidizing power, low cost, and relative nontoxicity [9, 10]. However, the rapid recombination of electrons and holes is one of the main reasons for the low photocatalytic efficiency of TiO2. Moreover, its wide band gap of 3.2 eV confines its application to the ultraviolet (UV) region, which makes up only a small fraction (≈5%) of the total solar spectrum reaching the earth’s surface [11]. In order to utilize irradiation from sunlight or from artificial room light sources, the development of visible-light-active TiO2 is necessary. In the past few years, carbon-based TiO2 photocatalysts have attracted cosmic interest for improved photocatalytic performance [12, 13]. Graphene, in particular, has been regarded as an extremely attractive component for the preparation of composite materials [14, 15]. In addition to its large theoretical specific surface area, graphene has an extensive two-dimensional π-π conjugation structure, which endows it with excellent conductivity of electrons [16]. Carriers in pristine graphene sheets have been reported to behave as massless Dirac fermions [17].

There was no statistical difference in mortality (p = 0.328) between the SAMU (1.5%) and CB (2.5%) groups, this being an important index for analysis. There was no difference between the services of SAMU and of CB regarding hospitalization and deaths. Analyzing the data according to the type of vehicle used, there are statistical differences

in deaths and hospital admissions associated with the use of the USA vehicle. In fact, in theory, more severe cases should be attended by this specialist team. Other details that draw attention relate to levels of severity of the trauma. Amongst all the scores for trauma severity analyzed (GCS, ISS, RTS and TRISS), there were no statistical differences between the groups studied, either for the overall averages or for the grouping into classes. However, the same was not true in the learn more analysis by type of vehicles; patients being treated by the USA vehicles showing the worst prognosis, according to the data found. A study conducted in Spain by Nieva et al [32] compared two models of emergency trauma care in two different towns: Pyrénées-Atlantiques (France) and Navarra (Spain). The authors found significant statistical differences in rescue times in APH, but comparable in-hospital mortality rates (p

= 0.138). In this study, the authors also report a statistical difference in the type of pre-hospital care; in France, according to the pre-hospital service index, 90.4% selleck products of patients receive direct care by an advanced support team, in medicalized ambulances or helicopters. In Spain, this index drops to 75.5% (p<0.001). One of the pillars in trauma care is the presence of quality standards for the care provided. Coimbra et al [11] and Fraga [33] state that in Brazil, there is no organized system for trauma care that covers all the different phases of care. They report that there are no epidemiological studies, no records of trauma at municipal and state levels, a lack Ketotifen of information regarding pre-hospital care, and a lack of coordination between hospitals of different complexities and the Institute

of Forensic Medicine, all of which pose barriers to a comprehensive study of the causes of death by external causes. In the present study, we analyze the patients who died. No statistical differences were found between the variables age, total time taken by the service, RTS, ISS and TRISS of patients attended by SAMU and CB. Unfortunately we do not have any data or information from other institutions that would enable a proper comparison with our data. This lack of statistical difference indicates that the pre-hospital system does not directly influence mortality, since there were no statistical differences, in this study, between the groups studied. When we look specifically at deaths, we see that the prognostic indices present statistical differences when compared with the survivors.

PubMedCrossRef 23. Topcu O, Kuzu I, Karayalcin K: Effects of peritoneal lavage with

scolicidal agents on survival and adhesion formation in rats. World J Surg 2006, 30:127–133.PubMedCrossRef 24. Jover R, Gutierrez A, Zarate V, et al.: Reduction of abdominal hydatid disease with prolonged treatment. Am J Gastroenterol 1997, 92:1231–1232.PubMed 25. Magistrelli P, Masetti R, Coppola R, et al.: Surgical treatment of hydatid disease of the liver: a 20-year experience. Arch Surg 1991, 126:518–523.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions OM conceived the idea of the study, and also performed and supervised the whole process and operated when required, written and Torin 1 concentration corresponded the manuscript. AH assisted in managing the patients with strict vigilance and helped in the preparation of manuscript. All authors read and approved the final manuscript.”
“Introduction and objective The main objective of wound repair

is to restore skin integrity and, while doing this to reduce rate of infection, scarring, and functional impairment [1]. Lacerations are repaired with sutures, staples, adhesive tapes, and tissue adhesives. Each method has its own advantages and disadvantages [2]. Suturing is the most commonly used method in laceration repair [3]. It is the strongest of all wound closure materials and allows best approximation of wound edges irrespective of wound shape. However, it selleckchem is also the most time-consuming and user-dependent among all techniques available. Repair via stapling is another method used for scalp lacerations. It is preferable to suturing in emergency services because it is a quicker and less painful procedure and associated with a lower cost and risk of needle stick injury to the operator. It is also preferred in pediatric age groups owing to the

above-mentioned Fossariinae properties [4–6]. Hair apposition technique is an alternative technique in scalp lacerations. Hair apposition technique was first defined by Hock et al. in 2002. In this technique, 4–5 strands of hair are grasped on each side of the wound. These strands are crossed once and a drop of glue is placed where the strands cross to secure the wound [7]. In this study, we aimed to compare the effectiveness of suturing, stapling, and hair apposition techniques used in repair of scalp lacerations in patients who presented to emergency department with scalp laceration. Materials and method This study was performed in a retrospectively at Numune Training and Research Hospital Emergency department between 01 January 2010 and 01 July 2010 after approval of the study by the local ethics committee (2010-33). Research carried out on humans must be in compliance with the Helsinki Declaration. Cosmetic problems, patient satisfaction, wound healing status, and complications were determined from the files of the patients who returned for follow-up examination on 7th and 15th days of suturing.

​1016/​j.​bbamem.​2012.​09.​017 16. Wolfe AJ: The acetate switch. Microbiol Mol Biol Rev 2005,69(1):12–50.PubMedCrossRef PI3K inhibitor 17. Gimenez R,

Nunez MF, Badia J, Aguilar J, Baldoma L: The gene yjcG, cotranscribed with the gene acs, encodes an acetate permease in Escherichia coli. J Bacteriol 2003,185(21):6448–6455.PubMedCrossRef 18. Jolkver E, Emer D, Ballan S, Krämer R, Eikmanns BJ, Marin K: Identification and characterization of a bacterial transport system for the uptake of pyruvate, propionate, and acetate in Corynebacterium glutamicum. J Bacteriol 2009,191(3):940–948.PubMedCrossRef 19. Kasianowicz J, Benz R, McLaughlin S: The kinetic mechanism by which CCCP (carbonyl cyanide m-chlorophenylhydrazone) transports protons across membranes. J Membr Biol 1984,82(2):179–190.PubMedCrossRef 20. Hosie AHF, Allaway D, Poole PS: A monocarboxylate permease

of Rhizobium leguminosarum is the first member of a new subfamily of transporters. J Bacteriol 2002,184(19):5436–5448.PubMedCrossRef 21. Oehmen A, Yuan Z, Blackall LL, Keller J: Comparison of acetate and propionate uptake by polyphosphate accumulating organisms and glycogen accumulating organisms. Biotechnol Chk inhibitor Bioeng 2005,91(2):162–168.PubMedCrossRef 22. Borghese R, Cicerano S, Zannoni D: Fructose increases the resistance of Rhodobacter capsulatus to the toxic oxyanion tellurite through repression of acetate permease (ActP). Antonie Van Leeuwenhoek 2011,100(4):655–658.PubMedCrossRef Elongation factor 2 kinase 23. Burow LC, Mabbett AN, McEwan AG, Bond PL, Blackall LL: Bioenergetic models for acetate and phosphate transport in bacteria important in enhanced biological phosphorus removal. Environ Microbiol 2008,10(1):87–98.PubMed Competing interests The authors declare that they have no competing interests. Authors contributions XS and KFK designed and carried out the studies and drafted the manuscript. JSHT conceived of the study, participated in the design and coordination of the study and drafted the manuscript.

All authors read and approved the final manuscript.”
“Background Bacteriophages have critically important roles in genome diversification and the evolution of virulence and host adaptation of enteric bacteria. Genes encoding Shiga toxins (Stx) 1 and 2 are found on lambdoid phages in Shiga-toxigenic Escherichia coli, while similar Gifsy and Fels phages encode a number of virulence factors in Salmonella enterica serovar Typhimurium. In addition to carrying genes encoding virulence factors, integrated prophage can affect gene expression of the host bacterium. The recent demonstration of three distinct bacteriophages integrated into the genome of Campylobacter jejuni chicken isolate RM1221 suggested that such phages may be common and important for the biology of C. jejuni[1]. At least one of these three C. jejuni integrated elements (CJIEs) [2] was a Mu-like phage inducible with mitomycin C designated CJIE1 (or Campylobacter Mu-like phage 1, CMLP1).

In hematologic neoplasms, MiRNA-29 expression levels are inversely correlated with prognosis of Mantle cell lymphoma (MCL) [12]. In addition, MiR-29 reduces cell growth and induces apoptosis in primary acute myeloid leukemia (AML) cells and related cell lines [13]. Moreover, it has been reported that by inhibiting MMP2 activity, MiR-29 plays an important inhibitory role in APOBEC3G induced colon cancer

migration and invasion [14]. Finally, consistent with the data from studies on other types of cancer, MiR-29 family inhibits ovarian cancer development Selleck U0126 by targeting DNA methyltransferases 3A and 3B [15]. Unfortunately, there is relatively lack of information on the role of MiR-29 in breast cancer. Study from JK Richer’s group demonstrated that Mir-29a has an inhibitory role in tumor growth in vivo [16]. However, in another paper, the authors showed that MiR-29a may promote metastasis through facilitating epithelial-to-mesenchymal transition [17]. Thus, the function of Mir-29 in tumorigenesis and metastasis of breast cancer still remains unclear. In the current study, we are endeavored to further elucidate the roles of MiR-29 in breast cancers, which highlights MiR-29 as a potential new biomarker and therapeutic target for breast cancer. Materials and methods Reagents Micro-RNA assays for mir-29a

(002112), mir-29b (000413), mir-29c (000587) and RUN48 (001006) were purchased from Applied Biosystems. Fetal bovine serum (FBS) was from GIBCO. SuperSignal Substrate Western blotting detection system was from Pierce (USA). PVDF membrane was Florfenicol purchased from Bio-Rad Midostaurin Inc. B-Myb antibody (05–175) and cyclin D1 antibody were purchased from Millipore. Cyclin A2 (ab32498) antibody and GAPDH antibody (ab9485) were purchased from Abcam. Luciferase Assay Kit and pMIR-REPORT System were purchased from Applied Biosystems. β-Gal Assay Kit was purchased from Invitrogen (K1455-01). Lipofectamine 2000 reagent was purchased from Invitrogen. Cell culture T-47D, MDA-MB-453, MCF-7 and MCF-10A cells were obtained from American Type Culture Collection. Human Mammary Epithelial Cells (HMEC) were purchased from Invitrogen (A10565). Cells

were maintained in their proper media recommended by the companies and placed in a humidified incubator with 5% CO2 and 95% air at 37°C. Plasmids and transduction A DNA fragment containing the hsa-miR-29a precursor (plus 100 bp upstream and 100 bp downstream) was amplified from genomic DNA of HMEC cells and cloned into pcDNA(+)3.1 vector (Invitrogen). The primers used here are: 5′-gaattcactcattccattgtgcctgg-3′ and 5′-ctcgagttgctttgcatttgttttct-3′. MiRZip-29a construct (MZIP29a-PA-1) and its vector control (SI505A-1) were obtained from System Biosciences. For the luciferase assay, pMIR-REPORT System (Applied Biosystems) was used. The plasmids (pMIR-REPORT-Luciferase-B-Myb-3′-UTR and its mutant) were constructed by following methodology. A 363-bp fragment (nt 2319–2681) of the 3′UTR of B-Myb (NM_002466.

In the light absorption spectra (shown in Figure 4a), it could be found that it is these nanoparticles that resulted in the enhancement of the light absorption of the devices. Figure 3 Surface SEM image, EDS spectrum, and XRD pattern of a CIGS layer. The CIGS layer was deposited at a substrate temperature Selleckchem BMN673 of 400°C for 3 min. (a) The surface SEM images of the CIGS layer, (b) the analysis results of the EDS spectrum of the

CIGS nanoparticle at the position marked by a white cross in (a), and (c) the XRD pattern of the CIGS layer shown in (a). Figure 4 Schematic of LSPR light trapping, UV-vis absorption spectra, and PL spectra. (a) Schematic of LSPR light trapping for a hybrid system of ITO/CIGS/P3HT:PCBM in which the CIGS nanoparticles are embedded between the ITO substrate and P3HT:PCBM photoactive layer. (b) The UV-vis absorption spectra of ITO/CIGS, ITO/P3HT:PCBM, and ITO/CIGS/P3HT:PCBM. (c) The PL spectra of ITO/P3HT:PCBM and ITO/CIGS/P3HT:PCBM. To investigate the effects

of the CIGS nanoparticles on the light absorption and charge separation efficiency of the conjugated polymer active layers, we measured the UV-visible-infrared absorption and PL spectra of the P3HT:PCBM layers with and without the CIGS interlayers (prepared on ITO-glass substrates). Figure 4b Dabrafenib displays the absorption spectra of CIGS/ITO, P3HT:PCBM/ITO, sum of CIGS and P3HT:PCBM, and P3HT:PCBM/CIGS/ITO. Obviously, the CIGS interlayer enhances the light absorption of the P3HT:PCBM active layer in the spectral range of 300 to 650 nm.

More importantly, the absorption intensity of P3HT:PCBM/CIGS/ITO is much larger than that of the sum of CIGS/ITO and P3HT:PCBM/ITO. It should be noted that the thickness of the P3HT:PCBM monolayer is approximately equal to that of the CIGS/P3HT:PCBM bilayer (about 100 nm) according to the cross-sectional SEM image (see Figure 2c), i.e., the enhancement of light absorption is not due to the thickness change of the P3HT:PCBM layer. Moreover, the CIGS interlayer absorbs only very little incident light. Therefore, most of the increased PAK6 absorption should come from the P3HT:PCBM close to the interfaces between the P3HT:PCBM and CIGS nanoparticles. The mechanism may be similar to the localized surface plasmon resonant (LSPR) effect [16–20]. It has been known that the excitation of the LSPR through the resonant interaction between the electromagnetic field of incident light and the surface charge of metallic nanostructures causes an electric field enhancement (that can be coupled to the photoactive absorption region) and increases the absorption of photoactive conjugate polymer or organic semiconductor [21–23]. The above results demonstrate that the semiconductor CIGS nanoparticles may also exhibit LSPR effect just as metallic nanostructures do.

Changes in expression of these components were quantified, and the findings are summarized in Figure 4C. Figure 4 Expression of proteins associated with the PI3K/Akt signaling and the intrinsic (mitochondrial) apoptotic pathways after varying times of treatment of CA46 cells with baicalin. (A) Expression of p-Akt in various untreated cell types as detected by phospho-Akt specific antibody. Lane 1, CA46 cells;

lane 2, Jurkat cells; lane 3, K562 cells; lane 4, HL-60 cells; lane 5, normal peripheral blood mononuclear cells-1; lane 6, normal peripheral blood Acalabrutinib nmr mononuclear cells-2. (B-E) CA46 cells were treated with 40 μM baicalin for the times indicated. Protein expression was analyzed by Western blotting. (B) Western

blot showing expression of β-actin, Akt, p-Akt, NF-κB, IκB, p-IκB, mTOR and p-mTOR. (C) Expression of p-Akt/Akt, NF-κB, IκB, p-IκB, and p-mTOR/mTOR relative to that of β-actin. (D) Western blot showing expression of β-actin, Bcl-2, Bax, cleaved caspase-9, cleaved caspase-3, and uncleaved (116 kD) and cleaved (85 kD) PARP. (E) Expression of cleaved caspase-9, cleaved caspase-3, uncleaved and cleaved PARP, Bax, and Bcl-2 relative to that of β-actin. Findings are representative of those obtained on three separate occasions. *P <0.05 compared to the 0 h control; † P <0.05 compared to 24 h treatment; ‡ P <0.05 compared to 48 h treatment. 5-Fluoracil clinical trial The profound decreases in expression of total cellular NF-kB and p-IkB, accompanied by significant increases in IkB expression, in response to baicalin treatment were interpreted to indicate a condition wherein nuclear NF-kB signaling should be dramatically impaired. Accordingly, expression of nuclear NF-kB was reduced by 25.8%, 50.4% and 65.4% at 24, 48 and 72 h of treatment with 40 μM baicalin, respectively Phenylethanolamine N-methyltransferase (not shown). Activation of

the intrinsic mitochondrial apoptotic pathway It was considered essential to ascertain whether baicalin suppresses proliferation of CA46 cells and promotes DNA fragmentation in these cells through activation of the intrinsic (mitochondrial) apoptotic pathway. To this end, expression of relevant apoptosis-related proteins was examined by Western blotting. Treatment with baicalin increased expression of the pro-apoptotic proteins Bax, activated (cleaved) caspase 3, activated (cleaved) caspase 9, and activated (cleaved) PARP. By contrast, expression of the anti-apoptotic protein Bcl-2 and of the inactive form of PARP was decreased following treatment with the drug (Figure 4D). Relative expression of these proteins after baicalin treatment was quantified, and findings are presented in Figure 4E.

However, inasmuch as these types of shifts in environmental conditions represent artificial in vitro manipulations that cannot fully mimic the spirochete’s natural habitats [37, 41, 42], there may be other aspects of RpoN-RpoS pathway activation that have not yet been appreciated using such in vitro culture conditions as surrogates for natural stimuli. In an attempt to garner more biologically relevant Selleck AZD2281 gene expression information and to determine at what specific

phase(s) of the enzootic life cycle of B. burgdorferi the RpoN-RpoS pathway is induced and may remain active, we examined the expression of rpoS and selected target genes of RpoS over the entire tick-mammalian enzootic life cycle. Results and discussion Although in vitro gene expression data have suggested that the RpoN-RpoS pathway is most robust at the tick-mammal transmission interface [9, 17, 21, 36, 38–40, 43], comprehensive gene expression analysis data to support this contention by assessing actual tick and mammalian tissues have been lacking. Furthermore, heretofore, activation of the pathway over the broader tick-mammalian cycle has not been assessed. To address this dearth of information, we examined the expression of rpoS throughout the complete infectious life cycle of B. burgdorferi. rpoS transcription is activated during tick feeding and remains active

during mammalian infection by B. burgdorferi R788 manufacturer In Cell press vitro, rpoS is markedly induced in spirochetes cultivated under conditions that largely mimic tick engorgement, suggesting that rpoS expression is robust during the early transmission phase. Herein, our qRT-PCR analyses indicated that, in larval ticks during acquisition, only 0.4 copies of rpoS transcripts per 100 flaB transcripts were detected in fed larvae, and no rpoS transcripts were detected in intermolt larvae (Figure 1A). However, when exposed to a blood meal, rpoS transcription

was dramatically induced; in nymphal ticks following 24, 48, or 72 hours of feeding, 1.8, 3.4, or 8.2 copies of rpoS transcripts per 100 flaB transcripts were detected, respectively (Figure 1A). These data suggest that RpoS is synthesized actively during nymphal tick feeding, and that RpoS then likely transcribes its gene targets. Previously, Caimano et al. [17] reported an increase in rpoS transcripts in engorged infected nymphs (collected at 6-8 days post feeding to repletion). Our more recent data not only are consistent with the findings of Caimano et al. [17], but further pinpoint that the activation of rpoS expression occurs initially in nymphal ticks upon blood feeding. Figure 1 qRT-PCR analysis of rpoS transcription in ticks and in mouse tissues. A, flat (uninfected) larvae, fed larvae, intermolt larvae, and fed nymphs during transmission phase were collected at 24-, 48-, and 72-h post-feeding. TT: tick transmission.

The primers Bfgi2_Int_F and Bfgi2_Int_R (Table 4) were designed directed outwards across the proposed attL and attR sites. Using these primers, amplification of product should only occur if a circularized form of Bfgi2 is present in the cell. The size (2.25 Kb) sequence of the resulting PCR product confirmed the presence of the circular intermediate (Fig. 6 panel B, Lane 3). Attempts to show plaque formation using NCTC9343 as

Cabozantinib supplier an indicator strain did not produce any visible plaques. This could be due to the phenomenon of limited host range for the bacteriophage. However, given that Bfgi2 circular intermediate was detected it is tempting to speculate that it is, or is a derivative of an active phage and such phage could be transmitted to a non-lysogenized strain of B. fragilis, bringing with

it a copy of a C10 protease. C10 protease genes are present in clinical isolates of B. fragilis and in the healthy human faecal microbiota In addition to the 3 genome strains, a panel of 5 clinical isolates of B. fragilis from ZD1839 several human infection sites (Table 7) were tested by allele-specific PCR for the C10 protease genes they harbour. The results indicated that this panel of strains have a complement of bfp genes more similar to NCTC9343 than to 638R (Table 1). The distribution of bfp genes in the clinical isolates is not identical, and none of the 5 isolates carried all four bfp genes. The bfp1-4 genes were detected in 3, 5, 1 and 0 clinical isolates respectively. The bfp4 gene was not be detected in any of these clinical strains, while bfp1 was not detected in two strains (NCTC 10584 and NCTC 11295). In contrast, bfp2 was encoded by all strains. In B. fragilis strain YCH46, there is a CTnERL-type conjugative transposon 353 bp distance from the bfi1A-bfp1-bfi1B gene cluster. However, this conjugative transposon is not present

in either of the other two sequenced B. fragilis genomes, 638R and NCTC 9343. The bfp3 gene was only detected in one clinical isolate (NCTC 9344), with a concomitant detection from of the Bfgi2 insertion. In all cases a 595 bp fragment was successfully amplified using the primer pair Bfgi2_attB_F and Bfgi2_attB_R (not shown), indicating the presence of a free integration site for Bfgi2 in all strains. It should be noted that for NCTC 9344 and 638R, there was a lower product yield and although not quantitative this is likely due to the integration of Bfgi2 in a sub-population of the cells. Table 7 Bacterial strains used in this study B. fragilis strain Source of isolate Reference 638R Clinical isolate, human [57] YCH46a Bacteraemia, human [19] NCTC9343 Appendix abscess, human [58] NCTC9344 Septic operation wound, human [59] NCTC10581 Empyema fluid, human [60] NCTC10584 Pus, human [58] NCTC11295 Pus from fistula, human [61] NCTC11625 Post-operative wound infection, human [62] a. Analysis of genome sequence only.

​who.​int/​malaria/​publications/​world_​malaria_​report_​2013/​en/​] URL 2. Ridley RG: Medical need, scientific opportunity and the drive for antimalarial

drugs. Nature 2002,415(6872):686–693. 10.1038/415686a11832957CrossRefPubMed 3. Bannister LH, Hopkins JM, Fowler RE, Krishna S, Mitchell GH: A brief illustrated guide to the ultrastructure of Plasmodium falciparum asexual blood stages. Parasitol Today 2000, 16:427–433. 10.1016/S0169-4758(00)01755-511006474CrossRefPubMed 4. Asahi H: Plasmodium falciparum : Chemically defined medium for continuous intraerythrocytic Opaganib supplier growth using lipids and recombinant albumin. Exp Parasitol 2009, 121:22–28. 10.1016/j.exppara.2008.09.00918851965CrossRefPubMed 5. Asahi H: Intraerythrocytic Plasmodium falciparum growth in serum-free medium with an emphasis on growth-promoting factors. In Malaria Parasites. Edited by: Okwa OO. Croatia: InTech, Rijeka; 2012:73–90. [ http://​www.​intechopen.​com/​books/​malaria-parasites]URL SRT1720 clinical trial 6. PlasmoDB. [ http://​plasmodb.​org/​plasmo/​]

7. Asahi H, Tolba MEM, Tanabe M, Ohmae H: Molecular factors that are associated with early developmental arrest of intraerythrocytic Plasmodium falciparum . Can J Microbiol 2013, 59:485–493. 10.1139/cjm-2013-016623826958CrossRefPubMed 8. Asahi H, Kanazawa T: Continuous cultivation of intraerythrocytic Plasmodium falciparum in a serum-free medium with the use of a growth-promoting factor. Parasitology 1994, 109:397–401. 10.1017/S00311820000806417800407CrossRefPubMed 9. Asahi H, Izumiyama S, Tolba ME, Kwansa-Bentum B: Plasmodium

falciparum : differing effects of non-esterified fatty acids and phospholipids on intraerythrocytic growth in serum-free medium. medroxyprogesterone Exp Parasitol 2011, 127:708–713. 10.1016/j.exppara.2010.11.00121095186CrossRefPubMed 10. Alvarez HM, Xue Y, Robinson CD, Canalizo-Hernandez MA, Marvin RG, Kelly RA, Mondragon A, Penner-Hahn JE, O’Halloran TV: Tetrathiomolybdate inhibits copper trafficking proteins through metal cluster formation. Science 2010,327(5963):331–334. 10.1126/science.1179907365811519965379CrossRefPubMedCentralPubMed 11. Ding X, Xie H, Kang YJ: The significance of copper chelators in clinical and experimental application. J Nutr Biochem 2011, 22:301–310. 10.1016/j.jnutbio.2010.06.01021109416CrossRefPubMed 12. Festa RA, Thiele DJ: Copper: an essential metal in biology. Curr Biol 2011, 21:R877-R883. 10.1016/j.cub.2011.09.040371800422075424CrossRefPubMedCentralPubMed 13. Turski ML, Thiele DJ: New roles for copper metabolism in cell proliferation, signaling, and disease. J Biol Chem 2009, 284:717–721. 10.1074/jbc.R800055200261360418757361CrossRefPubMedCentralPubMed 14. Markossian KA, Kurganov BI: Copper chaperones, intracellular copper trafficking proteins. Function, structure, and mechanism of action. Biochemistry (Mosc) 2003, 68:827–837. 10.1023/A:102574022888812948382CrossRef 15. Choveaux DL, Przyborski JM, Goldring JP: A Plasmodium falciparum copper-binding membrane protein with copper transport motifs.