The majority of vascular trauma in USA, South America and militar

The majority of vascular trauma in USA, South America and military conflict areas in Europe was penetrating trauma reaching up to 90% in some reports [15–17]. The actual incidence of vascular trauma in most European countries is unknown. Finland has an

annual incidence of 1.3 per 100,000 inhabitants while Sweden has an incidence of 2.3 per 100,000 inhabitants [9]. Our incidence of major vascular trauma due to road traffic collisions alone is 1.87 cases/100 000 inhabitants per year. The studies from Sweden and Finland included all vascular injury patients admitted to hospitals. About 20% were caused by blunt trauma. In contrast our study was limited only to hospitalized vascular injury in road traffic collisions. Only 34% of trauma in our community is caused by RTC which indicates that Momelotinib nmr vascular trauma in general is even much higher than Finland and Sweden [18]. It may be argued that the number of patients of this study is small. Nevertheless we think that the data was very accurate as it captured prospectively

all injuries in all age groups with their detailed mechanism of injury in a specific population over a specific time. Analyzing the biomechanics of crashes is important. About 90% of injuries can be clinically predicted if the biomechanics of RTC was well understood [19]. This will help reducing missed injuries. It is important to note that the majority of vascular injuries were in the upper part of the body selleck chemical (upper limb and thorax) similar to other studies [9, 12, 20]. All check details thoracic aortic injuries in our study occurred in pedestrians hit by moving vehicles. These are acceleration injuries in which the moving aortic arch is accelerated compared to the

fixed part. We have recently shown that injury severity of RTC patients was higher for non vehicle occupants especially pedestrians, who also accounted for most deaths [5]. The risk of thoracic aortic injury was significantly higher with side-impact crashes and particularly if the occupants were unbelted [21] because side impact hits the weak side of the vehicle. None of our car occupants was wearing seatbelts. If an occupant was not restrained and had a front impact collision, he/she will lean forward [22–24] and may try to protect him/herself with his/her upper limbs leading to their fracture and major vascular injuries of the upper limbs as they cannot tolerate the impact of energy Defining Selleck Hydroxychloroquine the incidence and mechanism of vascular trauma would help in adopting preventive strategies and directing resources in this part of the world. Trauma centers should be well equipped with an angiographic suite, interventional radiologists, and a vascular team to optimize clinical outcome of these life-threatening situations. The most affordable, effective and cheapest way to reduce the burden of injury is prevention [25]. Injury prevention is usually highly cost effective saving both medical costs and lives [26]. We should adopt an epidemiological approach if we are serious in preventing these injuries.

7% efficiency The fill factors were strongly dependent on the lo

7% efficiency. The fill factors were strongly dependent on the loading of the MS-275 in vitro carbon black powder and found to be around 68%. Interfacial charge transfer and mass transport were characterized by cyclic voltammetry and electrochemical impedance spectroscopy. This technique of synthesizing nanostructures for high surface area along with optimum carbon black loading afforded an effective and simple way to replace the Pt-based counter electrode for DSSC. Overall, the

TiO2/carbon black-based DSSC showed excellent cell efficiency that rivals cells with a Pt-based CE and exhibited remarkable electrocatalytic activity. This work provides an intriguing way of structurally designing a low-cost, Pt-free, high-performance CE material for DSSCs. Acknowledgements This work was financially supported by the MEST and KETEP JSH-23 manufacturer PRN1371 (MKE) grants (2012 K001288,

20120009633, and 20114030200010). References 1. O’Regan B, Grätzel M: A low-cost, high-efficiency solar cell based on dye-sensitized colloidal TiO2 films. Nature 1991, 353:737–740.CrossRef 2. Nazeeruddin MK, Kay A, Rodicio I, Humphry-Baker R, Müller E, Liska P, Vlachopoulos N, Graetzel M: Conversion of light to electricity by cis-X2bis(2,2′-bipyridyl-4,4′-dicarboxylate)ruthenium(II) charge-transfer sensitizers (X = Cl-, Br-, I-, CN-, and SCN-) on nanocrystalline TiO2 electrodes. J Am Chem Soc 1993, 115:6382–6390.CrossRef 3. Hagfeldt A, Grätzel M: Molecular photovoltaics. Acc Chem Res 2000, 33:269–277.CrossRef 4. Grätzel M: Photoelectrochemical cells. Nature 2001, 414:338–344.CrossRef 5. Lim J, Lee M, Balasingam SK, Kim J, Kim D, Jun Y: Fabrication of panchromatic dye-sensitized solar cells using pre-dye coated TiO2 nanoparticles by a simple dip coating technique. RSC Adv 2013, 3:4801–4805.CrossRef 6. Wu J, Hao S, Lan Z, Lin J, Huang M, Huang Y, Li P, Yin S, Sato T: An all-solid-state

dye-sensitized solar cell-based poly(N-alkyl-4-vinyl- pyridine iodide) electrolyte with efficiency of 5.64%. J Am Chem Soc 2008, 130:11568–11569.CrossRef 7. Saji VS, Jo Y, Moon HR, Jun Y, Song HK: Organic-skinned inorganic nanoparticles: GNA12 surface-confined polymerization of 6-(3-thienyl) hexanoic acid bound to nanocrystalline TiO 2. Nanoscale Res Lett 2011, 6:1–5.CrossRef 8. Ramkumar S, Anandan S: Synthesis of bianchored metal free organic dyes for dye sensitized solar cells. Dyes Pigm 2013, 97:397–404.CrossRef 9. Fan J, Hao Y, Cabot A, Johansson EMJ, Boschloo G, Hagfeldt A: Cobalt(II/III) redox electrolyte in ZnO nanowire-based dye-sensitized solar cells. ACS Appl Mater Interfaces 2013, 5:1902–1906.CrossRef 10. Kao MC, Chen HZ, Young SL, Lin CC, Kung CY: Structure and photovoltaic properties of Zno nanowire for dye-sensitized solar cells. Nanoscale Res Lett 2012, 7:1–16.CrossRef 11. Chiu PK, Cho WH, Chen HP, Hsiao CN, Yang JR: Study of a sandwich structure of transparent conducting oxide films prepared by electron beam evaporation at room temperature.

Infect Immun 1991, 59:1739–1746 PubMed 21 Hijnen M, van Gageldon

Infect Immun 1991, 59:1739–1746.PubMed 21. Hijnen M, van Gageldonk PG, Berbers GA, van Woerkom T, Mooi FR: The Bordetella pertussis virulence factor P.69 pertactin retains its immunological Fedratinib cost properties after overproduction in Escherichia coli. Protein Expr Purif 2005, 41:106–112.CrossRefPubMed 22. Lee SF, Halperin SA, Knight JB, Tait A: Purification and

immunogeniCity of a recombinant Bordetella pertussis S1S3FHA fusion protein expressed by Streptococcus gordonii. Appl Environ Microbiol 2002, 68:4253–4258.CrossRefPubMed 23. Roberts M, Fairweather NF, Leininger E, Pickard D, Hewlett EL, Robinson A, Hayward C, Dougan G, Charles IG: Construction and characterization of Bordetella pertussis mutants lacking the vir-regulated P.69 outer membrane protein. Mol Microbiol 1991, 5:1393–1404.CrossRefPubMed 24. Mattoo S, Cherry JD: Molecular

pathogenesis, epidemiology, and clinical manifestations of respiratory infections due to Bordetella pertussis and other Bordetella subspecies. Clin Microbiol Rev 2005, 18:326–382.CrossRefPubMed 25. Hellwig SM, Rodriguez ME, Berbers GA, Winkel JG, Mooi FR: Crucial role of antibodies to pertactin in Bordetella pertussis immunity. J Infect Dis 2003, 188:738–742.CrossRefPubMed 26. Cherry JD, Gornbein J, Heininger U, Stehr K: A search for serologic correlates of immunity to Bordetella pertussis cough illnesses. Vaccine 1998, 16:1901–1906.CrossRefPubMed 27. Storsaeter J, Hallander HO, Gustafsson L, Olin P: Levels of anti-pertussis antibodies learn more related to protection after household exposure to Bordetella pertussis. Vaccine 1998, 16:1907–1916.CrossRefPubMed 28. Ausiello

CM, Lande R, Stefanelli P, Fazio C, Fedele G, Palazzo R, Urbani F, Mastrantonio P: T-cell immune response assessment as a complement to serology and intranasal protection click here assays in determining the protective immunity induced by acellular pertussis vaccines in mice. Clin Diagn Lab Immunol 2003, 10:637–642.PubMed 29. Mills KH, Barnard A, Watkins J, Redhead K: Cell mediated immunity to Bordetella pertussis : role of Th1 cells in bacterial clearance in a murine respiratory infection model. Infect Immun 1993, 61:399–410.PubMed 30. Cheung GY, Xing D, Prior S, Corbel MJ, Parton R, Coote JG: Effect of different forms of adenylate cyclase toxin of Bordetella pertussis on protection afforded by an acellular pertussis vaccine in a murine model. Infect Immun 2006, 74:6797–6805.CrossRefPubMed 31. Medical MS-275 datasheet Research Council: Vaccination against whooping cough: relation between protection in children and results of laboratory tests. Br Med J 1956, 2:454–462.CrossRef 32. Guiso N, Capiau C, Carletti G, Poolman J, Hauser P: Intranasal murine model of Bordetella pertussis infection .I. Prediction of protection in human infants by acellular vaccines. Vaccine 1999, 17:2366–2376.CrossRefPubMed 33.

In this group of recruits,


In this group of recruits,

we this website found considerable dietary deficiency. First, despite the high check details energy needs during this period of training, the recruits consumed only 70% of the energy recommendations of the NSOR, with the NSF group reporting an 8.4% decrease in their BT total energy intake compared with the pre-induction total energy intake. This low intake may be explained by the presence of fundamental stressors in the military environment, such as periodic food restrictions, sleep deprivation, mental burden, and constant physical evaluations. These findings are in accordance with previous studies pointing to the fact that military personnel normally consume insufficient energy, whether or not they are provided with an adequate amount of food [33]. In this study, the deficient energy intake was not associated with a weight loss

but rather an increase of body weight during BT by 1.5%. This is also in line with previous studies, specifically that in this training program the gained weight was in lean body mass and not in fat [34]. We are concerned that our participants did not meet MDRI requirements. These deficiencies were observed for nearly every nutrient evaluated in the FFQ. The highest deficiencies were for vitamin D and calcium in the SF group, both around 60% of the MDRI before induction and click here also during BT. Of note, among the NSF group, vitamin D intake was the second most deficient variable, reported to be consumed at a level of 78.7% from MDRI before induction and at even a lower level of 59.6% during BT. In our

study, the SF recruits reported 41.0% less initial calcium and vitamin D intakes on induction day than the MDRI recommendations. Although vitamin D3 (cholecalciferol) is either formed in the skin after exposure to sunlight or obtained from nutritional sources, especially fatty fish [32], most IDF soldiers use Selleckchem ZD1839 sunscreen and wear long-sleeved clothing during military training. This may limit vitamin D3 synthesis, and therefore, the importance of balanced nutritional intake, especially of vitamin D and calcium, should be emphasized, even though we did not actually find low serum levels of vitamin D. Release of PTH is controlled by the level of calcium in the blood, with low blood calcium levels causing an increase in PTH. The main purpose of this hormone is calcium homeostasis. It is therefore not surprising that in these healthy young recruits, we did not find any pathological PTH or calcium values. A slight trend towards higher levels of PTH in the 4-month BT may represent a lack of dietary calcium. However PTH differences between SF and NSF or between induction values and 4 or 6 month values were not significant.

32-qter (17%) was observable in all passages of a series (case nu

32-qter (17%) was observable in all SB431542 mouse passages of a series (case number 445). The genomic region 1q21.1-qter frequently displayed gain. Changes in copy number were acquired during the growth period of xenografts including gains at 2q35-q37.3, 4q13.3-qter, 8p11.21-p21.2 and 8q and losses at 8p, 17p, 13, Xq21.1, 1p13.3-p31.1, 5q, 11q13.4-q24.3, Xq12-q26.3 and 16q. In one xenograft GSK2126458 research buy series (Case number 488), loss of 17q12-q21.32, that was present in the early passages, disappeared

during the growth process. The loss of 1p36.12-pter in the first two passages originating from lung metastasis (1 and 4) changed to loss of 1p36.21-pter in the last three passages (14, 21, and 30). The lung metastasis xenografts showed 9 copy number changes, whereas only 3 of these aberrations were observable in the xenograft passages from its primary tumor. Table 2 The copy number changes present in all the passages of each xenograft series Case No. (Nude) Array CGH results 488 (15) +1q21.1-qter, -13q14.12-qter

445 (22) -2q35-q37.3 (uncontinuous), + 8, +15, +17q21.32-qter 451 (53) -1q24.3-q25.2, – 3p12.3-p24.3, -9p21.3 455 (199) +1q, -16q, -9p21.3 430 (PRI) (230) -9p21.3 430 (MET) (248) -1p36.12-pter, -9p21.3 PRI = Primary Tumor, MET = Lung Metastasis Table 3 Copy number changes present in only part of the passages of each xenograft series Case Nude- Passage Array CGH result 488 15- 2, 4, 7, 11, 14 -2q35-q37.3 488 15- 1, 2, 4, 7 -17q12-q21.32 488 15- 14 +17 451 53- 11, 15,18, 21 +4q13.3-qter, -17p 455 199- 5, 11, 17, 25 -13 455 199- 25 -Xq21.1 430 (PRI) 230- SRT1720 nmr 1, 4, 9, 19 +8p11.21-p21.2, +8q 430 (MET) 248- 1, 4 -1p36.12-pter 430 (MET) 248- 14, 21, 30 -1p36.21-pter, -1p13.3-p31.1, -5q,     -11q13.4-q24.3, -Xq12-q26.3 430 (MET) 248- 21, 30 +8p11.21-p21.2, +8q 430 (MET) 248- 30 -16q PRI = Primary Tumor, MET = Lung Metastasis Figure 1 Copy number changes on each chromosome were ordered using hierarchical clustering. Most of the

xenograft passages of each series clustered together and also with the passage 0, its corresponding primary tumor. MicroRNA alterations in xenografts Differences in miRNA expression between xenografts and control samples were detected upon analysis (Figure 2). Exclusively expressed miRNAs were detected; two in control samples filipin (miR-31, miR-31*) and 46 in all xenograft passages (Table 4). In addition, 5 miRNAs (miR-106b, miR-93, miR-181b, miR-101, miR-30b) were significantly over-expressed (q-value < 0.05), while 6 miRNAs (miR-145, miR-193a-3p, miR-100, miR-22, miR-21, miR-574-3p) were significantly under-expressed across the xenograft passages in relation to the controls (q-value < 0.05). Xenografts from primary and control samples were compared to xenograft passages from the lung metastasis (Case number 430), to determine differences in miRNA expression.

The cut-off

The cut-off GS-9973 chemical structure frequency f T is defined as the

frequency at which the current gain becomes unity and indicates the maximum frequency at which signals can be propagated in the transistor. Once both gate capacitance and transconductance are calculated, f T can be computed using the quasi-static approximation [38, 39]. (15) It should be noted that a rigorous treatment beyond quasi-static approximation requires the inclusion of capacitive, resistive, and inductive elements in the calculation. In Figure 5, the quantity f T L G, where L G is the channel length, as function of V G, for increasing values of uniaxial tensile stain, is depicted. Assuming a channel length of less than L G=50 nm, f T Dactolisib exceeds the THz barrier

throughout the bias window, confirming the excellent high-frequency potential of GNRs. Furthermore, Figures 10 and 11 show the variation of cutoff frequency versus gate voltage and strain ε (in the on-state), respectively. We clearly observe that f T increases rapidly until the turning point ε≃7% and then decreases with lower rate for higher strain values (ε>7%). This is a direct consequence of both transconductance and gate capacitance variations with strain. Therefore, the high-frequency performance of AGNR-FETs improves with tensile uniaxial strain, before the LOXO-101 manufacturer ‘turning point’ of band gap variation but becomes worse after this point. Figure 10 Dependence of ( f T L G ) on V GS for various uniaxial strains. The drain voltage is held constant at 0.5 V. Figure 11 Variation of ( ) with uniaxial tensile strain in the ‘on-state’ V GS = V DS =0 . 5 V. Lastly, we study the effect of strain on the switching performance of the DG-GNR FET. Figures 12, 13, and 14 show the dependence of I on, I off and I on/I off ratio on the uniaxial

tensile strain, respectively. As it is clearly seen, the variation of both I on and I off is opposite to the variation of the band gap with strain whereas Adenosine triphosphate the ratio I on/I off changes with strain following the band gap variation. The on-current I on changes almost linearly with strain whereas the I off and the ratio I on/I off changes almost exponentially with strain. Note that the corresponding curves are not symmetric around the turning point, e.g., although for ε=12%, the GNR band gap returns to its unstrained value; the drain current at this stain value does not completely return to that of the unstrained GNR. This can be explained by the fact that although the band gap has returned its unstrained value, the carrier group velocity has been modified because, under tensile strain, some C-C bonds of the AGNR have been elongated [9]. Figure 15 shows the I on versus I on/I off plots for various strains which provides a useful guide for selecting device characteristics that can yield a desirable I on/I off under strain.

Antonie Van Leeuwenhoek 2008, 94:11–19 PubMedCrossRef 8 Meschke

Antonie Van Leeuwenhoek 2008, 94:11–19.PubMedCrossRef 8. Meschke H, Walter S, Schrempf H: Characterization and localization of prodiginines from Streptomyces lividans suppressing Verticillium dahliae in the absence

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R: Specificity and function of mycorrhization helper Selleck GSK461364 bacteria (MHB) associated with the Pseudotsuga menziesii-Laccaria laccata symbiosis. Symbiosis 1992, 14:335–344. 15. Lehr NA, Schrey SD, Bauer

R, Hampp R, Tarkka MT: Suppression of plant defense response by a mycorrhiza helper bacterium. New Phytol 2007, 174:892–903.PubMedCrossRef 16. Riedlinger J, Schrey SD, Tarkka MT, Hampp R, Kapur M, Fiedler H-P: Auxofuran, a novel substance stimulating growth Rebamipide of fly agaric, produced by the mycorrhiza helper bacterium Streptomyces AcH 505. Appl Environ Microbiol 2006, 72:3550–3557.PubMedCrossRef 17. Maier A, Riedlinger J, Fiedler H-P, Hampp R: Actinomycetales bacteria from a spruce stand: characterization and effects on growth of root symbiotic and plant parasitic soil fungi in dual Batimastat manufacturer culture. Mycol Progr 2004, 3:129–136.CrossRef 18. Conrath U, Pieterse CM, Mauch Mani B: Priming in plant-pathogen interactions. Trends Plant Sci 2002, 7:210–216.PubMedCrossRef 19. Conn VM, Walker AR, Franco CM: Endophytic actinobacteria induce defense pathways in Arabidopsis thaliana. Mol Plant Microbe Interact 2008, 21:208–218.PubMedCrossRef 20. Lehr NA, Schrey SD, Hampp R, Tarkka MT: Root inoculation with a forest soil streptomycete leads to locally and systemically increased resistance against phytopathogens in Norway spruce. New Phytol 2008, 177:965–976.PubMedCrossRef 21. Lehr N-A, Adomas A, Asiegbu F, Hampp R, Tarkka MT: WS-5995 B, an antifungal agent inducing differential gene expression in the conifer pathogenHeterobasidion annosum but not in Heterobasidion abietum. Appl Microbiol Biotechnol 2009, 85:347–358.

Eukaryot Cell 2003,

2:306–317 CrossRefPubMed 34 Crudden

Eukaryot Cell 2003,

2:306–317.PLX-4720 concentration CrossRefPubMed 34. Crudden G, Chitti RE, Craven RJ: Hpr6 (heme-1 domain protein) regulates the susceptibility of cancer cells to chemotherapeutic drugs. J Pharmacol Exp Ther 2006, 316:448–455.CrossRefPubMed 35. Oakley F, Meso M, Iredale JP, Green K, Marek CJ, Zhou X, May MJ, Millward-Sadler H, Wright MC, Mann DA: Inhibition of inhibitor of kappaB kinases stimulates hepatic stellate cell apoptosis and accelerated recovery from rat liver fibrosis. Gastroenterology 2005, 128:108–120.CrossRefPubMed 36. Greupink R, Bakker GDC-0973 price HI, Reker-Smit C, van Loenen-Weemaes AM, Kok RJ, Meijer DK, Beljaars L, Poelstra K: Studies on the targeted delivery of the antifibrogenic compound mycophenolic acid to the hepatic stellate cell. J Hepatol 2005, 43:884–892.CrossRefPubMed 37. Hagens WI, Mattos A, Greupink R,

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The Co layer, E A is set at θ = 0°, 30°, 60°, and 90° in the simu

The Co layer, E A is set at θ = 0°, 30°, 60°, and 90° in the simulations, respectively. Compared with the single-layer dots, the stray fields from the uncompensated magnetic poles in the Co layer influence the magnetization reversal of the Fe layer drastically. A strong E A direction dependence of the Fe layer hysteresis loops for the circle trilayer dot is illustrated in Figure 3. As is shown, H c, M r/M s, H n, and H a are all affected. When θ = 0°, 30°, and 60°, a shift of the loop center along the field axis is obvious, which reflects the interlayer interaction directly [18–20]. The bias field H B of the Fe layer is defined from the two H n here, i.e.,

H B = (H n1 + H n2)/2, to evaluate the interaction strength, where H n1 and H n2 are LY2835219 cost the nucleation field of the descending and ascending branches of the loop. The bias field depending on θ is displayed in Figure 4 for different asymmetric dots. It is clearly seen that with θ increasing, H B decreases monotonically, which can be interpreted intuitively from the viewpoint of magnetic poles on the Co layer edge. However, a simple fitting with the relationship of

H B(θ) = H B(0)cosθ failed quantitatively, as also shown in the Figure. A detailed inspection in the magnetization reversal elucidates that a new S-state is formed before it evolves to a vortex in the

circle dot. This S-state is the straight result in the Fe layer to respond the Co magnetic poles. A magnetization reversal Evofosfamide process through the S-state of a circle dot with θ at 30° is depicted in Figure 5, in which the S-state is indicated in Figure 5c. For the semicircle dots, the shape anisotropy is sufficiently strong to dominate their Fenbendazole magnetization process in spite of the Co poles, leading to undetected bias effect. Figure 3 Fe layer minor loops of circle trilayer dots on easy axis direction of Co layer. The Co layer easy axis deviates from the applied field direction by the angle of 0°, 30°, 60°, 90°. The loop of a single Fe layer dot is also presented. Figure 4 The Fe layer bias field as a function of the easy axis direction of Co layer. The Co layer easy axis deviates from the applied field direction by the angle of 0°, 30°, 60°, 90°. The asymmetric dots are characterized by α = 0, 0.25, 0.5, 0.75, 1. The dash line denotes a cosine function fitting for the circle dots. Figure 5 Snapshots of magnetization reversal process through S-state of a circle dot with θ at 30°. The applied field is (a) 2,500, (b) 560, (c) 180, (d) 160, (e) - 2,320, and (f) - 2,500 Oe. The dot shows saturation, S-, vortex, and reverse saturation states in sequence. The interlayer dipolar interaction influences the stabilizing range of the Fe vortex as well.

2736 strains after irradiation

with 60, 80, 100 and 120 k

2736 strains after irradiation

with 60, 80, 100 and 120 keV/μm (LETs) and 60 MeV/u (energy) 12C6+-ions are compared. (D) Surviving fraction of D. natronolimnaea svgcc1.2736 strains after irradiation with 60, 80, 100 and 120 keV/μm (LETs) and 90 MeV/u (energy) 12C6+-ions are compared. Interpretation of the parameter fitting RBE/LET dependencies in this study indicating an increased RBE is not unique for carbon ions of charged particle radiation. The RBE values derived from the survival curves support the known dependence of RBE on LET, particle species and dose [36]. For 12C6+ ions, the transportation safety technologies Etomoxir datasheet (TST)-calculated RBE/LET dependencies gradually increase with increasing LET until they reach a maximum value, after which they slowly decrease [37]. The dependencies rely strongly on the particular physical characteristics of the ion beam determined for example by the Selisistat energy and LET of the particles

under consideration [38]. This is demonstrated in Figure 1 (A, B, C and D), where survival curves of D. natronolimnaea svgcc1.2736 cells after irradiation with 60, learn more 80, 100 and 120 keV μm-1 (LET) and 30, 45, 60 and 90 MeV u-1 (energies) 12C6+ ions are compared. Each survival curve has been constructed using a linear-quadratic model [39]. RBE decreases with increasing particle energy [40], and the same increased ionization density should hold true for all cell types [41]. Because the 12C6+ ions have a higher energy for any given LET, lower energy density and thus lower RBE result. One must bear Florfenicol in mind, however, that high ionization densities will lead to more extensive damage that is more difficult to repair. Cellular defects arising from damage repair may not necessarily translate into increased effectiveness because even simple damage is not always repairable by the cell [42, 43]. Survival data of the D. natronolimnaea svgcc1.2736 cells were plotted using a logarithmic function of the surviving fraction versus dose. For comparison purposes the curves were represented mathematically, based on hypothetical models for the mechanisms associated with lethality.

Interpretation of the shape of the survival curve is still in question, as is the best way to mathematically present these types of data sets. The interpretation of the shape of the cell survival curve is still debated, as is the best way to fit these types of data mathematically. As already indicated in Figure 1A-D, after reaching a maximum at 120 keV μm-1 surviving fraction not further increases, but instead decreases towards higher dose values. For the 12C6+ heavy ion irradiation (A dose of ≥2.5 Gy for ≥45 MeV u-1) surviving fraction values as low as 1% are observed. The strain cells survival as a function of dose follows almost exponential behaviour, and thus survival curves are generally shown in Figure 1A-D.