Discussion The structural characterization of samples etched at d

Discussion The RG-7388 structural characterization of samples etched at different etching times provides additional insight to the mechanism of formation of the mesoporous SiNWs on highly boron-doped Si by the single-step MACE process. In principle,

MACE involves two successive processes: surface nucleation of metal catalysts (e.g., Ag) and anisotropic Si etching. Si dissolution takes place through oxidation by H2O2 and oxide dissolution in HF. Metal nucleation occurs preferentially at surface states and sites around the dopants. Since the oxidation donates four electrons, while Ag+ ion reduction consumes only one electron, a space charge is formed by the excess electrons on the surface that electrically drives Ag+ ions to diffuse toward the nuclei for reduction. Alternate oxidation and nucleation cycles induce sinking of the Ag particles into the Si substrate, resulting in Si etching and SiNW formation. These nanowires are vertical to the OSI-906 clinical trial Si substrate. The morphology and texturing of the SiNWs depend strongly on the original Si wafer resistivity. SiNWs from resistive Nirogacestat Si wafers have

in general a smooth surface and a crystalline core without pores. On the other hand, Si wafers with a resistivity of less than approximately 5 mΩ·cm produce mesoporous SiNWs. This was demonstrated for both p-type [11] and n-type Si wafers [12, 19]. Since dopants are additional preferential sites for the nucleation of Ag particles, their high density induces porosification of the Si substrate and the formation of a mesoporous layer at the Etofibrate interface between the SiNWs and the crystalline Si substrate. Our experiments showed that the thickness of this

porous Si layer increases with the increase of the etching time. It was also deduced from our PL experiments (this is discussed below) that the initial porosity of this layer was lower than that of the SiNWs. Furthermore, the porosity of the SiNWs was gradually increasing from their bottom to their top (different pore and nanocrystal sizes). These observations led us to the conclusion that the formation of the porous Si layer underneath the SiNW arrays precedes the SiNW formation. The SiNWs are thus porous from the beginning, while additional porosification of the nanowires takes place during etching. The higher porosity of the tops of the SiNWs is attributed to the longer time into the etching solution and is responsible for the saturation of the process after a certain time. Indeed, we observed that after the 60-min etching time, it was not possible to further increase the SiNW length. This is attributed to the fact that part of their tops is fully dissolved in the solution when the porosity of this part of the nanowires becomes high enough. From that time on, although the etching process continues on the Si surface, the SiNW length does not increase, since the nanowire tops are progressively dissolved in the solution.

Conservative treatment in salvageable solid visceral injury in pr

Conservative treatment in salvageable solid visceral injury in primary blast injury in our setting is restricted as a lack of easy availability of advanced imaging techniques and intensive care unit, sophisticated resuscitation measures and the invasive eFT-508 datasheet monitoring INCB28060 cell line facilities. Moreover, multiple organ injury in a number of individual patients in this series did not favored conservative management in our settings. Laparotomy continues to be decisive factor in final diagnosis. Conclusion PBI causes varied abdominal organ injuries. Single or multiple organ damage can be there. Intestines

as well as solid viscera are prone for damage. Small intestine is commonest viscera damaged. Multiple perforations are present commonly in a small gut. An awareness of presentation of pattern of injuries occurring in a primary injury can make early diagnosis. Observation period for those who have been very close to the site of blast

even without any evident injury is quite important, as it is GSK2245840 supplier not only the pallets but also even the blast waves, falling of objects, stampede which can inflict very serious trauma to these patients. Most of the times laparotomy may reveal even the most concealed injuries. References 1. Ritenour AE, Baskin TW: Primary blast injury: update on diagnosis and treatment. Crit Care Med 2008,36(7 Suppl):S311–7.CrossRefPubMed 2. Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV: Blast injuries. Lancet 2009,1;374(9687):405–15.CrossRef 3. Champion HR, Holcomb JB, Young LA: Injuries Methane monooxygenase from explosions: physics, biophysics, pathology, and required research focus. J Trauma 2009,66(5):1468–77.CrossRefPubMed 4. Guzzi LM, Argyros G: The management of blast injury. Eur J Emerg Med 1996, 3:252–5.CrossRefPubMed 5. Cripps NPJ, Cooper GJ: Risk of late perforation in intestinal contusions caused by explosive blast. Br J Surg 1997, 84:1298–303.CrossRefPubMed 6. Ignjatović D: Vojnosanit Pregl. 2.Blast injuries of the intestines

in abdominal injuries. 1994,51(1):3–1. 7. Carter PS, Belcher PE, Leicester RJ: Small-bowel adhesions long after blast injury. J R Soc Med 1999,92(3):135–6.PubMed 8. De Palma RG, Burris DG, Champion HR, Hodgson MJ: Blast Injuries current concepts. N Engl J Med 2005, 352:1335–42.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions IW: took acquisition of data, compilation of relevant literature, formatting, revision, drafted the preliminary and final manuscript. FQ: helped in drafting, acquisition and revision of manuscript TS, RW AA, and IG:helped in acquisition of data and revision of manuscript. MN:helped in final drafting and revision of manuscript. All authors have read manuscript and approved the final version of manuscript.

Patients were divided according to CyA administration frequency—o

Patients were divided according to CyA administration frequency—once a day (group 1) or twice a day (group 2). In each therapeutic response, there was no significant difference However, the time-to-remission curve analyzed using the Kaplan–Meier technique revealed a significant deference in cumulative CR rate (p = 0.0282; Fig. 3a) but not in cumulative CR + ICR1 rate (p = 0.314, Fig. 3b). Fig. 3 Probability of cumulative complete remission (CR) (a) and CR + incomplete remission 1 (ICRI) (b) for patients treated with PSL and CyA. Group 1 showed a significantly higher rate of CR (a) but not of CR + ICRI (b) compared with group 2

Assessment of clinical parameters After CyA + PSL treatment, the levels of UP, serum albumin, and serum total cholesterol significantly improved in both groups; however, there were no significant differences in each parameter

4SC-202 ic50 between the 2 groups. selleck products Serum creatinine level slightly increased in both groups CP673451 cell line but was not significant. Two patients in each group exhibited a doubling of serum creatinine, around 2 mg/dL, at 48 weeks, although the levels were within the reference range at the start of treatment. At baseline, only 1 patient had mild hypertension in group 2 (155/89 mmHg), but the blood pressure normalized later. At the final observation, another patient in group 2 showed mild hypertension (150/88 mmHg). No patient had CyA-induced hypertension in either group. As the supportive therapy for MN, angiotensin II receptor blockers (4 and 2 patients in groups 1 and 2, respectively) Parvulin and angiotensin-converting enzyme inhibitors (one in group

1) and a combination of both (one in each group) were administered. However, these drugs did not produce any adverse effects including hyperkalemia. Although four patients in groups 1 and 2 showed mild hyperglycemia by steroids treatment, respectively, this did not have any serious influences on the results. Blood CyA concentrations The flowchart of the study design regarding assignment by blood CyA concentrations at 2 h post dose (C2) is shown in Fig. 4. Fig. 4 Flowchart of the study design: assignment by CyA blood concentrations at 2 h post dose (C2) Absorption profiles of CyA in groups 1 and 2 There were significant differences in AUC0–4 between groups (group 1 vs group 2: 3678 ± 181 vs 2506 ± 164 ng h/mL, p < 0.0001). In comparisons between AUC0–4 and CyA concentrations at each time point (C0–C4), C2 was most strongly correlated with AUC0–4 in the total patients (r = 0.032, 0.609, 0.780, 0.654, 0.579 for C0, C1, C2, C3, C4, respectively). Average C0 and C2 and the cut-off level for CR The average C0 and C2 during treatment were significantly correlated with the C0 and C2 at the AP, respectively (C0: r = 0.516, p = 0.0036; C2: r = 0.638, p = 0.0001). The average C2 in group 1 was significantly higher than in group 2; however, the average C0 in group 1 was significantly lower than in group 2.

Setting the appropriate threshold

Setting the appropriate threshold selleck products values and making identification rules for target detection are specific challenges, which can be overcome by the means of bioinformatics. In our study, the final identification of a bacterial pathogen was based on one to three different

oligonucleotides on the microarray. All these were spotted as duplicates and all of which, with the exception of CNS, were required to pass threshold values set for their positive identification. When more pathogens are included on the array, the designing of the probes, the setting of threshold values [22], and formulation of identification rules will require PX-478 research buy intensive testing. The testing procedure can be enhanced by automated data analysis, which provides objective and reproducible interpretation of the AZD6094 research buy results. In our study, the Prove-it™ Advisor software generated data analysis for reporting and allowed effective data management and tracking. We evaluated the assay by comparing its results with those of sepsis diagnostics, although other applications using specimens from normally sterile site of the body are feasible as well. Our sample material consisted of 186 blood culture samples and

causative agents were identified originally in 69 of these samples. These positives corresponded to nine of the targets on the assay pathogen panel. However, some of the targets in the pathogen panel, A. baumannii, H. influenzae, L. monocytogenes, and N. meningitidis, were not present in any of the samples and no false identifications of these bacteria

were made. When comparing these data with those of the blood culture results, discrepancies were observed due to the limited numbers of CNS probes on the panel, or for unknown reasons. The CNS probes on the panel were selected to cover the two most clinically prevalent CNS species S. haemolyticus and S. saprophyticus, and the most virulent species S. lugdunensis. If more CNS species were needed Methocarbamol to be covered by the assay, their respective probes could be designed and added to the CNS probe panel [23]. Such species could be S. pasteuri, S. capitis and S. hominis all three of which were present in the blood cultures analyzed in our study. We encountered some challenges with reconciling the microarray image analyses data and building optimal detection rules for the precise identification of all the pathogens. These specific problems are illustrated by missing or suboptimal duplicates causing false negative identifications. The microarray image and data analysis present commonly acknowledged challenges, especially when the microarray data quality is not optimal. For instance, the distinction between the actual spots and artifacts on the array, or the gridding of the image can be problematic [24]. These challenges in automated image and data analyses together with result reporting could be a reason for the current lack of available microarray-based diagnostics.

1 (3 1) −2 1 (−3 2– − 0 9)* SF-36#  Physical function 80 5 (8 2)

1 (3.1) −2.1 (−3.2– − 0.9)* SF-36#  Physical function 80.5 (8.2) 96.6 (5.7) 16.1 (12.9–19.3)* 69.8 (22.8) 94.7 (8.1) 24.9 (19.8–30.0)*  Physical role 80.4 (32.8) 93.1 (19.2) 12.7 (1.3–24.1)* 56.6 (43.5) 93.4 (19.6) 36.8 (26.4–47.2)*  Bodily pain 71.9 (12.8) 90.3 (12.7) 18.4 (11.5–25.3)* 64.3 (19.1) 92.1 (9.9) 27.8 (23.2–32.4)*  General health 48.2 (18.3) 75.0 (13.7) 26.8 (19.2–34.4)*

52.6 (18.7) 76.7 (15.0) 24.1 (18.4–29.8)*  Social function 92.0 (11.6) 91.3 (13.2) −0.70 (−7.8–6.4) 74.5 (20.4) 90.6 (11.8) 16.1 (11.0–21.2)*  Emotional role 95.2 (17.8) 96.7 (15.3) 1.5 (−6.9–9.9) 82.0 (32.9) 91.8 (23.5) 9.8 (1.0–18.6)*  Mental health 80.6 (11.3) 72.4 (10.2) −8.2 (−13.8– − 2.6)* 73.7 (13.7) 71.0 (9.0) −2.7 (−6.3–0.9)  Vitality 66.4 (13.2) 69.1 (11.5) 2.7 (−3.6–9.0) 59.8(16.6) 66.0 (13.0) 6.2 (1.6–10.8)* Differences between early OA (CHECK) and healthy workers

* p < 0.05; Obeticholic concentration Daporinad in vitro # mean (SD) Health status comparison The subjects with OA reported statistically significantly lower scores than the healthy workers on the physical component of SF-36, for both sexes. old Because of the higher mean age and the small number of the male subjects with OA, afterwards a corrected analysis was performed, in which they were compared to an age-matched subsample of 30 healthy workers (mean age 58). Table 2 FCE performances of male subjects with early OA (CHECK, n = 15) and male healthy workers (n = 183) FCE test Age category # (years) Early OA mean (SD) Healthy workers mean (SD) Mean difference healthy—early OA (95% CI) Lifting low (kg) 45–54 31.8 (7.4) 44.9 (12.3) 13.2 (1.0–25.4)* 55–65 34.1 (6.1) 43.0 (14.5) 9.0 (3.5–14.4)* All 33.5 (6.3) 44.3 (13.0) 10.9 (7.0–14.8)* Lifting selleckchem Overhead (kg) 45–54 19.8 (2.9) 20.1 (4.8) 0.4 (−4.4–5.2) 55–65 17.3 (3.9) 18.9 (4.6) 1.6 (−1.4–4.5) All 17.9 (3.7) 19.7 (4.8) 1.8 (−0.7–4.3) Carry 2 hand (kg) 45–54 46.3 (13.4) 46.4 (11.0) 0.1 (−11.0–11.3) 55–65 35.7 (11.5) 43.1 (12.7) 7.4 (−0.9–15.7) All 38.5 (12.5) 45.4 (11.7) 7.0 (0.7–13.1)* Overhead work (s) 45–54 236 (103) 269 (127) 33 (−93–160) 55–65 207 (61) 270 (102) 63 (−0.4–127.1) All 214 (72) 270 (119) 55 (−7–117) Dynamic bend (s) 45–54 51 (7) 47 (6) −4 (–11–3) 55–65 62 (16) 66 (128) 4 (−74–82) All 60 (15) 48 (7) −12 (3–21)* Rep.

After washing with PBS, the labeled

After washing with PBS, the labeled Trichostatin A manufacturer cells were observed using a laser confocal scanning microscopy (LCM 510 Meta Duo Scan, Carl Zeiss, Oberkochen, Germany). Flow cytometry ADS, 12DD, 21DD, and NC were prepared for integrin β1 marker. A number of 1 × 106 cells were incubated with PE-conjugated integrin β1 antibodies at 37°C for 1 h in the dark. Then the cells were centrifuged and washed in PBS three times. Finally, cells were acquired by use of a FACScan (Becton Dickinson, Franklin Lakes, NJ, USA) flow cytometer running its accompanying CellQuest software. Statistical analysis All data were mean values ± standard deviation (SD). Statistical analysis

was performed using one-way analysis of variance test (SPSS17.0), with P < 0.05 regarded as statistical

significance. Results Detection of SOX9, COL II, COL I, and Aggrecan genes by real-time RT-PCR We used real-time RT-PCR to detect the expression of SOX9, COL II, COL I, and Aggrecan genes from the following nine groups: ADSCs group (ADS), normal chondrocytes group (NC), 3-day differentiation group (3DD), 6-day differentiation group (6DD), 9-day differentiation group (9DD), 12-day differentiation group (12DD), 15-day differentiation group (15DD), 18-day differentiation group (18DD), and 21-day differentiation group (21DD) (Figure 1). After addition of inducing medium, the expression of COL II, SOX9, and Aggrecan mRNA began to increase gradually, reaching a peak similar to that of NC at 12th MEK162 day. At 18th day, expression of these genes dropped to the level of the 6th day. Change of COL I mRNA was clearly detected until in group 15DD. Its expression was sevenfold higher than in ADS and maintained at high levels through day 21. These results indicate

that ADSCs after 12 days of differentiation express most of the chondrocytic gene markers, suggesting that they have differentiated into normal chondrocytes. After differentiating into mature chondroid cells, the expression of the markers was reduced gradually and over time dedifferentiation began. Figure 1 Gene expression analysis during chondrogenesis of ADSCs. ADSCs were Decitabine cultured for up to 21 days. RNA extracts at day 0, 3, 6, 9, 12, 15, 18, and 21 were analyzed for gene expression of SOX9, COL II, COL I, and Aggrecan normalized to NC, respectively. Asterisk Selleckchem Dibutyryl-cAMP indicates P < 0.05 (vs. NC) as determined by one-way analysis of variance. Atomic force microscopy analysis Cell topography The topography and the three-dimensional morphology of cells could be observed through AFM. Both 12DD and NC both took the shape of an irregular triangle or polygon with a flat and extended nucleus (Figure 2, E1, E2, I1, and I2). It was difficult to distinguish 12DD and NC by appearance. ADS cells were an irregular, long spindle shape with one round and extruded nucleus (Figure 2, A1 and A2).

Wren BW: The yersiniae – a model genus to study the rapid evoluti

Wren BW: The yersiniae – a model genus to study the rapid evolution of bacterial pathogens. Nat Rev Microbiol 2003,1(1):55–64.PubMedCrossRef 3. Chain PS, Carniel E, Larimer FW, Lamerdin J, Stoutland PO, Regala WM, Georgescu AM, Vergez LM, Land ML, Motin VL, et al.: Insights into the evolution of Yersinia pestis through whole-genome comparison with Yersinia pseudotuberculosis . Proc Natl Acad Sci USA 2004,101(38):13826–13831.PubMedCrossRef 4. Hinchliffe SJ, Isherwood KE, Stabler

RA, Prentice MB, Rakin A, Nichols RA, Oyston PC, Hinds J, Titball RW, Wren BW: Application of DNA microarrays to study the evolutionary genomics of Yersinia pestis and Yersinia pseudotuberculosis . Genome Res 2003,13(9):2018–2029.PubMedCrossRef Oligomycin A supplier 5. Sokurenko EV, Hasty DL, Dykhuizen DE: Pathoadaptive mutations: gene loss and variation in bacterial pathogens. Trends Microbiol 1999,7(5):191–195.PubMedCrossRef 6. Torres AG, Vazquez-Juarez RC, Tutt CB, ABT-263 ic50 Garcia-Gallegos JG: Pathoadaptive mutation that mediates adherence of shiga toxin-producing Escherichia coli O111. Infect Immun 2005,73(8):4766–4776.PubMedCrossRef 7. Day WA Jr, Fernandez RE, Maurelli AT: Pathoadaptive mutations that enhance virulence: genetic organization of the cadA regions of Shigella spp. Infect Immun 2001,69(12):7471–7480.PubMedCrossRef 8. Sun YC, Hinnebusch BJ, Darby C: Experimental evidence for negative selection in the evolution of a Yersinia pestis pseudogene. Proc

Natl Acad Sci USA 2008,105(23):8097–8101.PubMedCrossRef 9. Erickson DL, Jarrett CO, Callison JA, Fischer ER, Hinnebusch

BJ: Loss of a biofilm-inhibiting glycosyl hydrolase during the emergence of Yersinia pestis . J Bacteriol 2008,190(24):8163–8170.PubMedCrossRef 10. Rosqvist R, Skurnik M, Wolf-Watz H: Increased virulence of Yersinia pseudotuberculosis by two independent mutations. Nature 1988,334(6182):522–524.PubMedCrossRef 11. Bliska JB, Copass MC, Falkow S: The Yersinia pseudotuberculosis adhesin YadA mediates intimate bacterial attachment to and entry into HEp-2 cells. Infect Idelalisib chemical structure Immun 1993,61(9):3914–3921.PubMed 12. Isberg RR, Falkow S: A single genetic locus encoded by Yersinia pseudotuberculosis permits invasion of https://www.selleckchem.com/products/OSI-906.html cultured animal cells by Escherichia coli K-12. Nature 1985,317(6034):262–264.PubMedCrossRef 13. Isberg RR, Leong JM: Multiple β1 chain integrins are receptors for invasin, a protein that promotes bacterial penetration into mammalian cells. Cell 1990,60(5):861–871.PubMedCrossRef 14. Clark MA, Hirst BH, Jepson MA: M-cell surface β1 integrin expression and invasin-mediated targeting of Yersinia pseudotuberculosis to mouse Peyer’s patch M cells. Infect Immun 1998,66(3):1237–1243.PubMed 15. Hamburger ZA, Brown MS, Isberg RR, Bjorkman PJ: Crystal structure of invasin: a bacterial integrin-binding protein. Science 1999,286(5438):291–295.PubMedCrossRef 16. Leong JM, Fournier RS, Isberg RR: Identification of the integrin binding domain of the Yersinia pseudotuberculosis invasin protein. Embo J 1990,9(6):1979–1989.PubMed 17.

Global Environment Monitoring Unit—Joint Research Centre of the E

Global Environment Monitoring Unit—Joint Research Centre of the European Commission, Ispra Italy. http://​gem.​jrc.​ec.​europa.​eu/​ Overmars KP, Verburg PH (2005) Analysis of land-use drivers at the watershed and household level: linking two paradigms at the Philippine forest fringe. Int J Geograph Inf Sci 19:125–152CrossRef Pontius

RG, Cornell JD, Hall CAS (2001) Modeling the spatial pattern of land-use change with GEOMOD2: application and validation for Costa Rica. Agric Ecosyst Environ 85:191–203CrossRef Ramankutty N, Gibbs HK, Achard F, Defries R, Foley JA, Houghton RA (2007) Challenges to estimating carbon emissions from tropical deforestation. #click here randurls[1|1|,|CHEM1|]# Glob Change Biol 13:51–66CrossRef Salubrinal price Reid R, Gichohi H, Said M, Nkedianye D, Ogutu J, Kshatriya M, Kristjanson P, Kifugo S, Agatsiva J, Adanje S, Bagine R (2008) Fragmentation of a Peri-Urban Savanna, Athi-Kaputiei Plains, Kenya. In: Galvin KA, Reid RS, Behnke RH Jr, Thompson Hobbs N (eds) Fragmentation in semi-arid and arid landscapes. Springer, Dordrecht,

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At entry to the cohort, patients were aged 71 8 ± 12 7 years; the

At entry to the cohort, patients were aged 71.8 ± 12.7 years; they had BMI of 25.5 ± 5.3 kg/m2, and 15 % were classified as obese

(Table 1). The rate of smoking was 20 %. Time since diagnosis of osteoporosis was 21.5 ± 49.2 months. About half were receiving cardiovascular ATM Kinase Inhibitor manufacturer treatments such as antihypertensives or platelet Gilteritinib order inhibitors. Two thirds of the patients were receiving calcium and vitamin D supplementation. Fig. 1 Patient flow. MI myocardial infarction, UTS CPRD up-to-standard Clinical Practice Research Datalink (data) Table 1 Characteristics of the cohort of women with treated osteoporosis at cohort entry date, and for women receiving strontium ranelate and women receiving alendronate at date of initiation of treatment   Women with treated

osteoporosis Women receiving strontium ranelate during follow-up Women receiving alendronate during follow-up N = 112,445 N = 6,487 N = 94,654  Age, years 71.8 ± 12.7 74.9 ± 11.5 72.0 ± 12.5  Body mass index, kg/m2 25.5 ± 5.3 24.6 ± 5.0 25.5 ± 5.3  Smoking 22,820 (20 %) 894 (14 %) 18,554 (20 %) Characteristics of osteoporosis  Time since diagnosis, months 21.5 ± 49.2 (median, 0.4) 43.6 ± 57.5 (median, 21.3) 23.2 ± 49.1 (median, 0.5)  Calcium supplementation at entry 75,631 (67 %) 4,786 (74 %) 64,721 (68 %)  Vitamin D supplementation at entry 69,079 (61 %) 4,614 (71 %) 61,139 learn more (65 %) History of cardiovascular events  Myocardial infarction 4,502 (4 %) 309 (5 %) 3,740 (4 %)  Acute ischaemic cardiac eventa 6,524 (6 %) 447 (7 %) 5,464 (6 %) Treatments at entry see more  Antidiabetic agents 6,747 (6 %) 343 (5 %) 5,806 (6 %)  Statins/fibrates 26,510 (24 %) 1,710 (26 %) 23,503 (25 %)  Antihypertensive agents 57,546 (51 %) 3,472 (54 %) 48,861 (52 %)  Platelet inhibitors (including aspirin)

27,381 (24 %) 1,723 (27 %) 23,248 (25 %) Values are means ± SD or numbers (%) aCardiovascular procedure or ischaemic cardiac event (myocardial infarction, acute coronary syndrome, or unstable angina) During the follow-up period, 6,487 patients received strontium ranelate and 94,654 received alendronate. The mean cumulative exposure for strontium ranelate was 12.8 ± 16.4 months (with a maximum of 87 months), while that for alendronate was 25.4 ± 26.0 months. The patients receiving strontium ranelate were older than the general cohort of women with treated osteoporosis and had a longer time since diagnosis; they were also more likely to be receiving concomitant supplementation with calcium and vitamin D (Table 1). There were 1,352 cases of first definite MI in the cohort of women with treated osteoporosis (IR 3.24 per 1,000 patient-years; 95 % CI, 3.07–3.41). Of these, 16 cases were excluded from the analysis due to failure to identify six to ten matching controls, leaving 1,336 cases and 13,330 matching controls.

Acknowledgments This research is supported by the Environment Res

Acknowledgments This research is supported by the Environment Research and Technology Development Fund (A-1103 and S-6-1) of the Ministry of the Environment, Japan. We are also grateful to the participants for this comparison study. Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, LY333531 and reproduction in any medium, provided the original author(s) and the source are credited. References Akashi O, Hanaoka T (2012) Technological feasibility and costs of achieving

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B, Leimbach M, Bauer N (2010) ADAM’s modeling comparison project—intentions and prospects. Energy J 31:7–10. doi:10.​5547/​ISSN0195-6574-EJ-Vol31-NoSI-1 Grubb M, Carraro C, Schellnhuber J (2006) Technological change 2-hydroxyphytanoyl-CoA lyase for atmospheric stabilization: introductory overview to the innovation modeling comparison project. Energy J, Special Issue #1, 1–16. doi:10.​5547/​ISSN0195-6574-EJ-VolSI2006-NoSI1-1 Hanaoka T, Kawase R, Kainuma M, Matsuoka Y, Ishii H, Oka K (2006) Greenhouse gas emissions scenarios database and regional mitigation analysis. CGER-D038-2006. National Institute for Environmental Enzalutamide concentration Studies, Tsukuba. http://​www.​cger.​nies.​go.​jp/​publications/​report/​d038/​all_​D038.​pdf Hanaoka T, Kainuma M, Matsuoka Y (2009a) The role of energy intensity improvement in the AR4 GHG stabilization scenarios. Energ Effic 2(2):95–108. doi:10.