Kirk et al. 2001, 2008 Ascomata perithecial or rarely cleistothecial, sometimes clypeate, mostly globose, thick-walled, immersed or erumpent, black, sometimes setose, peridium composed of pseudoparenchymatous find more cells, pseudoparaphyses trabeculate or cellular, asci cylindrical, fissitunicate, with a well-developed ocular chamber, rarely with a poorly defined ring (J-), ascospores hyaline to brown, septate, thin or thick-walled, sometimes muriform, usually with sheath, anamorphs hyphomycetous or coelomycetous. Boehm et al. 2009a, b; Mugambi

and Huhndorf 2009b; Schoch et al. 2009; Shearer et al. 2009; Suetrong et al. 2009; Tanaka et al. 2009;

Zhang et al. 2009a Hemibiotrophic, saprobic, hypersaprobic, or lichenized. Habitats in freshwater, marine or terrestrial environment. Ascomata perithecioid, rarely cleistothecioid, https://www.selleckchem.com/products/Trichostatin-A.html immersed, erumpent to superficial, globose to subglobose, or lenticular to irregular, with or without conspicuous papilla or ostioles. Ostioles with or without periphyses. Peridium usually composed of a few layers of cells with various shapes and structures. Hamathecium persistent, filamentous, very rarely decomposing. Asci bitunicate, fissitunicate, cylindrical, clavate to obclavate, with or without pedicel. Ascospores hyaline or pigmented, ellipsoidal, broadly to narrowly fusoid or filiform, mostly septate. Pleosporales was formally established by Luttrell and Barr

(in Barr 1987b), characterised by learn more perithecioid ascomata, usually with a papillate apex, ostioles with or without periphyses, presence of cellular pseudoparaphyses, bitunicate asci, and ascospores of various shapes, pigmentation and septation (Table 1). Eighteen families were included, i.e. Arthopyreniaceae, Botryosphaeriaceae, Cucurbitariaceae, Dacampiaceae, Dimeriaceae, Hysteriaceae, Leptosphaeriaceae, Lophiostomataceae, Parodiellaceae, Phaeosphaeriaceae, Phaeotrichaceae, GBA3 Pleomassariaceae, Pleosporaceae, Polystomellaceae, Pyrenophoraceae, Micropeltidaceae, Tubeufiaceae and Venturiaceae. Recent phylogenetic analysis based on DNA sequence comparisons, however, indicated that separation of the orders (Pleosporales and Melanommatales) based on the Pleospora or Sporormia centrum type, is not a natural grouping, and Melanommatales has therefore been combined under Pleosporales (Liew et al. 2000; Lumbsch and Lindemuth 2001; Reynolds 1991). Six more families, i.e. Cucurbitariaceae, Diademaceae, Didymosphaeriaceae, Mytilinidiaceae, Testudinaceae and Zopfiaceae, were subsequently added to Pleosporales (Lumbsch and Huhndorf 2007).

Figure 3 Voltage evolution in PSi Er doping using a high constant current intensity. The presence of a double transient is evident. In the inset, the first derivative of the curve (blue dotted line, right axis) is shown superposed to the original

curve (red dotted line, left axis) to highlight the slope change induced by the presence of the double transient. To gain further insight in the differences between ST and DT regimes, we studied the evolution of the first stages of the doping process by means of GEIS. GEIS spectroscopy is a very useful technique with high sensitivity to surface changes and well suitable to the characterization of porous materials: it allows analyzing the response of the samples under a wide frequency window. KU55933 selleck inhibitor Moreover, the equivalent circuit approach was used to interpret the mechanism of the process. Parallel–series combinations of circuital electrical elements are used to simulate the response. Resistors (R) and capacitors (C) are mainly

adopted but also constant phase element (CPE) is often used, instead of C, to take account for possible non-ideality of the capacitor behavior: their admittance BI 10773 manufacturer is expressed by Y = Q (jω) n , the value of n being 1 for perfect capacitors [18]. Figure 4a shows an example of the typical Nyquist plot obtained during a low current doping: the data are the empty circles while the full line represents the results of the fitting obtained L-NAME HCl by the equivalent circuit in the inset. Starting from the high frequency range (left side), a first semicircle is easily individuated which may be attributed to the response of the bulk silicon, not involved in the doping process; the second semicircle, at intermediate

frequency, may be attributed to the response of the PSi layer. A linear trend about 45° sloped may be individuated in the last part of the spectrum, at the lowest frequencies, as well as a third semicircle, less defined with respect to the previous ones, attributable to diffusion of Er+3 ions which tend to accumulate near the pore surface. Figure 4 Comparison between fitted circuit models and measured Nyquist data obtained during doping at low (a) and high (b) current intensities. The equivalent circuit adopted is also shown as inset. Experimental data are the 4th and 3rd GEIS cycles of Figures 5a and 6b, respectively. Analogous discussion may be done on data obtained during high current doping (Figure 4b): in this case, the final part of the spectrum is better resolved and a further semicircle clearly appears. As shown in the inset of Figure 4b, a further circuital element was needed in the equivalent circuit to fit the related experimental data: a Warburg element W, corresponding to a CPE with n = 0.5 [18]. Different processes can be evocated to interpret this behavior, also considering the high values of cell potential which establish at high current.

P196 Laurans, L. P165 Laurent, C. O168 Laurent, J. O74 Laurent-Matha, V. P42 Laval, S. O84 Lawrence, J. O160, P77, P119 Lazar, A. O70 Lazarov, E. O12 Lazarovici, P. O115 Lazennec, G. O30 Le Guelte, A. P145 Le Mével, B. O107 Lear, R. O187 Lederman, H. P77 Lee, B.-H. P197 Lee, H.-Y. P19

Lee, I. J. P198 Lee, I. K. P86, P117 Lee, J. P19 Lee, K.-D. P129 Lee, K. O27, O28 Lee, S. H. P130 Lee, S. K. P154 Lee, Y. M. P130 Leek, R. O126 Leelahavanishkul, Go6983 supplier K. P40 Lefebvre, O. P65 LeFloch, R. O7 Lefort, E. P20 Legrand, E. P188 Lehne, F. P92 Lehner, M. P170 Leibovich-Rivkin, T. O14 Leibovici, J. O155, P143 Leiser, Y. O115 Lenain, C. P224 Leone, G. P155 Leonetti, C. P161 Leong, H. P131 Lepreux, S. P182 Lequeux, C. P214 Lerner, I. O95, O149, P142 Leroy-Dudal, J. P72 Lewis, C. O144 Lewis, J. D. O131, Fedratinib clinical trial O170, P76, P131, P179 Li, F. O158, P155 Li, B. O42 Li, H. O39 Li, J. O126 Li, J. O22 Li, L.-Y. O34 Li, N. P177 Li, X. O171 Li, X. O181 Li, X. P82 Li, X. O39 Li, Y. P41 Li, Y. O121, P184 Liang, H. O79 Liaudet-Coopman, E. P42 Libby, T. E. P58 Liekens, S. P21 Lieuwes, N. G. O57 Lin, D. O178 Lindahl, G. O129 Linde, N. O17, P87 Linderholm, B. P98 Selleck Sirolimus Lindner, D. P185 Lino, M. O25 Lionel, A. O174 Lionne-Huyghe, P. O48 Lis, R. P88 Lisanti, M. P. O184 Lishner, M. P7, P112 Littlefield,

B. P209 Liu, D. P209 Liu, G.-S. P208 Liu, M. P23 Liu, Q. P39 Liu, X. P177 Lo, S.-H. P223 Lobo, D. N. P2 Locke, J. A. P80 Logothetis, C. J. P217

Look, M. P. P79 Lopategi, A. O35, P123, P172, P219 Lopez-Perez, T. P156 Lorusso, G. O74 Lou, Q. O178 Lou, Y.-M. O56 Louderbough, J. P89 Louie, E. O55 Lu, H. O58 Lu, J.-F. P217 Lucien, F. P90 Lundin, S. O109 Luo, P. O98 Luo, X. P29 Lupu, R. O22 Lustgarten, J. P150 Luyt, L. O131, P179 Ly, E. P134 Lyden, D. O148, O160, P77, P119 Lyra, E. C. P22 Ma, Y. P171 Mac Gabhann, F. P207 MacDonald, J. P181 Mach, P. P120 Machelon, V. O86 Maciel, M. S. P22 Mack, A. P204 Mackensen, A. P49 Mackey, M. P138 Maity, G. O172 Maity, S. P217 Maizner, second E. P91 Majima, M. O165 Maldonado-Lagunas, V. P156 Malesci, A. P166 Maman, S. O120, P71 Mami-Chouaib, F. O106, P62 Manchester, M. O131 Mandapathil, M. O73, P178 Manfait, M. P134 Mann, L. O20 Mannello, F. P43 Mantovani, A. O46, O140, P166 Maoz, M. O26 Marangoni, E. O66 Marchetti, D. O113 Margaryan, N. O6 Margreiter, R. P53 Maria Carraro, D. P31 Mariani, P. P69 Marincola, F. M. O29 Marko, M. O88 Marongiu, F. O161 Marquez, J. P172 Marshall, D. P221 Martens, U. P78 Martin, K. O99 Martina, E. O25 Martinet, L. P173 Martini, V. P202, P203 Martino, E. P30 Martinoli, C. O64 Martowicz, A. P92 Masereel, B. O57 Masiero, M. O23 Mason, S. O169 Massagué, J. O169 Massamiri, T. P181 Masson, O. P42 Massonnet, G. O66 Matrisian, L. M.

The Lactobacillus sp. indicated by the black arrow, initially present both in the luminal and the mucosal microbial community, were lost during the treatment. On the contrary, the treatment selectively enhanced those species within the dashed square, species that preferentially adhere to the simulated gut surface. These molecular data showed that by means of an HMI module connected to the SHIME, it was possible to evaluate the modulating effect of the test product both on the luminal and mucosa-associated microbiota. The latter was different from the luminal one (in terms of relative abundance of the main species) as the mucin layer is colonized by a biofilm with bacterial species that

specifically (i) adhere to mucins, (ii) metabolize mucins learn more or (iii) proliferate in mucus due to the microaerophilic conditions at the bottom of this layer. This is also the case in vivo, where it was shown for instance that the mucosa-associated microbiota differs from the dominant fecal microbiota in both healthy subjects and patients with IBD [46]. Figure 5 DGGE fingerprinting analysis for bifidobacteria (a) lactobacilli (b) and composite data set of the gels for bifidobacteria. lactobacilli and total bacteria,

including bootstrap analysis with 1000 samplings (c). A = control period (Cluster II); B = treatment period (Cluster I). L = luminal samples collected from the SHIME reactor; CH5424802 M = mucus sample collected from a fraction of the membrane inside the HMI module. 0, 24 and 48 indicate the hours that the HMI modules have been connected to the SHIME system during the control and treatment periods (as illustrated in Figure 3). not Clustering analysis was based on the Pearson product–moment correlation coefficient and dendrograms were created by using UPGMA linkage. Finally, the positioning of two specific microbial groups (i.e. bifidobacteria and Faecalibacterium prausnitzii) in the mucus layer as analysed by FISH, provided an additional proof of the VX-689 purchase validity of the HMI module as compared to the in vivo situation (Figure 6). While the strict anaerobic bifidobacteria

tended to colonize the upper side of the mucus layer, F. prausnitzii mainly occurred in the lower part of the mucus, i.e. at the anoxic/oxic interphase (Figure 6a). Khan et al. demonstrated that F. prausnitzii can grow in the oxic-anoxic interphase due to the fact that this microorganism, despite being oxygen sensitive, copes with O2 because of a special extracellular electron shuttle of flavins and thiols [47]. Similar to the in vivo situation – where small amounts of oxygen permeate from blood vessels towards the gut lumen – in the HMI module, oxygen diffusion from the aerobic lower chamber to the anaerobic upper chamber (Figure 1) probably results in microaerophilic conditions at the base of the biofilm, allowing for F. prausnitzii to specifically colonize this niche. The qPCR data showed a decreasing concentration of F.

Since 2005, most human cases in China have been caused by B. melitensis biovar 3 [10]. Classical typing systems are unable to subdivide Brucella isolates below the biovar level. Molecular typing methods such as MLVA have been utilized to distinguish between strains of the same biovar in both animal and human isolates www.selleckchem.com/products/Roscovitine.html [3, 5, 6, 11–13]. In an effort to assess the value of MLVA as a subtyping tool for Brucella strains, genotypic characteristics of 105 B. melitensis isolates were investigated. Cluster analysis of these China strains, based on the eight variable-nucleotide

tandem repeat loci included in the MLVA-16 panel 1 grouped them all into the B. melitensis ‘East Mediterranean group’ [3] and unique from circulating strains in Northern Africa, Southern Europe (‘West Mediterranean group’ and ‘American group’). For instance, Alvocidib chemical structure an (panel 1 genotype 42 and 43) clustered separately from most of the other ‘West Mediterranean group’ (panel 1 genotype 49 and 51) and ‘American group’(panel 1 genotype 47). Previous studies have shown that Near Eastern countries frequently report human cases

associated with genotypes 42 and 43 [3, 14]. Genotype 42, as we have shown, is widely distributed throughout China, and has previously been reported to be predominant in Turkey, Portugal and Spain [13]. In Spain, human B. melitensis strains clustered into genotypes 42 (Eastern Mediterranean group, 55%), 48 and 53 (Americas group, ~11%) and 51 (Western Mediterranean group, ~8%). Chinese B. melitensis are classified in limited number of closely related genotypes showing variation mainly at the panel 2B loci. In China, the Inner Mongolia Autonomous Region is the most severe endemic focus of brucellosis, with an annual incidence

of the disease varying from 40 to 70/100,000 this website during 2005-2010 [2]. Inner Mongolia is in close proximity to Heilongjiang, Jilin, Hebei and Shanxi provinces; these provinces are located in the north and east of China, where stocking raising is the most important aspect of the economy. In these regions, B. melitensis genotype 42 strains were predominant, but genotype 42 strains were also common in provinces reporting sporadic cases such as Liaoning, Shandong, Zhejiang, Fujian and Tianjin. These isolates were only single-locus or double-locus variants of B. melitensis from the endemic regions. Of particular note is the apparently stability of genotype 42 in China; genotype 42 strains were isolated from Inner Mongolia in1957 as well as 53 years later. Guangdong province, which is now considered to be an endemic region for brucellosis, is located in the southern coastal region of China, where the A-1210477 cost incidence of human brucellosis has increased gradually since 2000. The prevailing panel 1 type is genotype 42 as well. The genotypes for most of the B. melitensis isolates in this series and their close relatedness by MLVA (single-locus variants and in some cases double-locus variants) compared to the relatedness of B.

In this study, we proposed a precautionary rule to guide our EPs and prevent CT misinterpretation. Through this study, we hope to contribute to the establishment of a safe and effective selleck chemicals emergency CT interpretation system for use in blunt trauma patients. Materials and methods Our emergency department (ED) is equipped with a multi-slice CT machine Selleck CCI-779 (from Toshiba Medical Systems Corporation) with 64 channels and is always in a state of standby for trauma patients. In blunt trauma, the EP in charge of the ED carries out a primary survey based on a standardized protocol, which actively employs whole body CT. EPs

interpret the CT scan at the time of imaging and record their image diagnoses in an electronic clinical chart. From there, the hospital procedure to definitive diagnosis based on CT is as follows. A radiologist interprets the emergency CT obtained in the ED within several hours, and this image report is uploaded to the electronic clinical chart. Every morning, the EPs discuss the radiologist’s report in a trauma conference and then arrive at a final CT diagnosis. To reduce CT misinterpretation by EPs, we established a simple precautionary rule, which advises EPs to interpret CT scans with particular care when a complicated injury is

suspected per the following criteria: 1) unstable physiological condition; 2) suspicion Selleckchem GNS-1480 of injuries in multiple regions of the body (e.g., brain injury plus abdominal injury); 3) high energy mechanism of injury; and 4) requirement

for rapid movement to other rooms for invasive treatment. If a patient meets at least one of these criteria, the EP should carefully interpret the CT scan. Namely, the EP should Farnesyltransferase undertake the following actions: 1) employment of enhanced CT for chest, abdomen, and pelvis; 2) re-interpretation of the images more than twice after short intervals; 3) changing the window levels according to the organs interpreted; 4) evaluation using not only an axial view but also a sagittal or coronal view when necessary; 5) use of a three-dimensional view to evaluate bone injuries; and 6) repetition of the CT after time has passed. Additionally, our rule specifies that the EP should request real-time interpretation by a radiologist in difficult cases per the following guidelines: 1) the patient’s physiological condition deteriorates in spite of treatment; 2) laboratory data show the development of anemia or metabolic acidosis in spite of treatment; or 3) unclear points remain in spite of re-interpretation or repetition of the CT. We posted this rule in the CT control room and the ED conference room, and we held a briefing session for our EPs introducing this new rule. We implemented the practice that the EP in charge of the ED must follow the rule. Our precautionary rule is shown in Table  1.

PubMedCrossRef 5. Datta SR, Brunet A, Greenberg ME: Cellular survival: a play in three Akts. Genes Dev 1999, 13:2905–2927.PubMedCrossRef 6. Kastan MB, Onyekwere O, Sidransky D, Vogelstein B, Craig RW: Participation of p53 protein in the cellular response see more to DNA damage. Cancer Res

1991, 51:6304–6311.PubMed 7. Mansur CP: The regulation and function of the p53 tumor suppressor. Adv Dermatol 1997, 13:121–166.PubMed 8. Sandor J, Ambrus T, Ember I: The function of the p53 gene suppressor in carcinogenesis. Orv Hetil 1995, 136:1875–1883.PubMed 9. Schoneich C: Protein modification in aging: an update. Exp Gerontol 2006, 41:807–812.PubMedCrossRef 10. Liu D, Xu Y: p53, oxidative stress, and aging. Antioxid Redox Signal 2011, 15:1669–1678.PubMedCentralPubMedCrossRef 11. Gottlieb TM, Oren M: p53 in growth control and neoplasia. Biochim Biophys Acta 1996, 1287:77–102.PubMed 12. Levy N, Yonish-Rouach E, Oren M, Kimchi A: Complementation by wild-type p53 of interleukin-6 effects on M1 cells: induction of cell cycle exit and cooperativity with c-myc suppression. Mol Cell Biol 1993, 13:7942–7952.PubMedCentralPubMed www.selleckchem.com/products/i-bet151-gsk1210151a.html 13. Vennstrom B, Sheiness D,

Zabielski J, Bishop JM: Isolation and characterization of c-myc, a cellular homolog of the GSK2118436 supplier Oncogene (v-myc) of avian myelocytomatosis virus strain 29. J Virol 1982, 42:773–779.PubMedCentralPubMed 14. Pelengaris S, Khan M, Evan G: c-MYC: more than just a matter of life and death. Nat Rev Cancer 2002, 2:764–776.PubMedCrossRef 15. Vita M, Henriksson M: The Myc oncoprotein as a therapeutic target for human cancer. Semin Cancer Biol 2006, 16:318–330.PubMedCrossRef heptaminol 16. Meyer N, Penn LZ: Reflecting on 25 years with MYC. Nat Rev Cancer 2008, 8:976–990.PubMedCrossRef 17. Amati B, Alevizopoulos K, Vlach J: Myc and the cell cycle. Front Biosci 1998, 3:D250-D268.PubMed 18.

Dang CV: c-Myc target genes involved in cell growth, apoptosis, and metabolism. Mol Cell Biol 1999, 19:1–11.PubMedCentralPubMed 19. Eilers M: Control of cell proliferation by Myc family genes. Mol Cells 1999, 9:1–6.PubMed 20. Jung P, Hermeking H: The c-MYC-AP4-p21 cascade. Cell Cycle 2009, 8:982–989.PubMedCrossRef 21. Gartel AL, Ye X, Goufman E, Shianov P, Hay N, Najmabadi F, Tyner AL: Myc represses the p21(WAF1/CIP1) promoter and interacts with Sp1/Sp3. Proc Natl Acad Sci U S A 2001, 98:4510–4515.PubMedCentralPubMedCrossRef 22. Müller D, Bouchard C, Rudolph B, Steiner P, Stuckmann I, Saffrich R, Ansorge W, Huttner W, Eilers M: Cdk2-dependent phosphorylation of p27 facilitates its Myc-induced release from cyclin E/cdk2 complexes. Oncogene 1997, 15:2561–2576.PubMedCrossRef 23. Sherr CJ, Roberts JM: CDK inhibitors: positive and negative regulators of G1-phase progression. Genes Dev 1999, 13:1501–1512.PubMedCrossRef 24. Strasser A, Harris AW, Bath ML, Cory S: Novel primitive lymphoid tumours induced in transgenic mice by cooperation between myc and bcl-2. Nature 1990, 348:331–333.PubMedCrossRef 25.

This effect was slightly stronger for the chemically deacetylated alginate from P. aeruginosa SG81 than for the alginate of the O-acetylation mutant P. aeruginosa FRD1153. This might be explained by the fact that the alginate of P. aeruginosa FRD1153 still contained a residual of 9% (w/w) of O-acetyl groups,

whereas the chemically deacetylated alginate of P. aeruginosa SG81 was free of O-acetyl groups [24]. No protection of lipase activity was obtained by the addition of dextran and minor in the presence of algal alginates. Xanthan showed comparable protection ability as the bacterial alginate of P. aeruginosa SG81. These results were in accordance with the finding that the lipase did not see more or only slightly Selonsertib bind to these polysaccharides at a concentration of 1 mg/ml in the microtiter plate assay (Figure 2). Table 2 Inactivation temperatures of lipase LipA calculated by extrapolation of the linear gradient of the heat inactivation curves Sample T100 T50 T0 (°C) (°C) (°C) Tris–HCl buffer (control) 45.0 +/− 2.5 63.8 +/− 1.1 82.7 +/− 2.9 Alginate FRD1 45.1 +/− 3.5 72.2 +/−

2.6 101.7 +/− 2.8 Alginate FRD1153 47.3 +/− 2.2 76.7 +/− 1.2 106.2 +/− 3.2 Alginate SG81 47.9 +/− 2.5 70.3 +/− 3.3 91.0 +/− 3.0 Alginate SG81, deacetylated 49.2 +/− 3.5 78.5 +/− 1.9 109.0 +/− 3.0 Algal alginate 54.0 +/− 4.7 68.1 +/− 2.7 87.2 +/− 3.4 Dextran 46.1 +/− 3.2 66.1 +/− 3.2 86.2 +/− 3.4 Xanthan 47.8 +/− 3.9 74.1 +/− 1.5 95.4 +/− 2.7 The lipase activity was detected after 20 min incubation at different temperatures in the presence (1 mg/ml) and absence of polysaccharides. Three independent experiments were performed in duplicates. Shown are

T0 representing the temperature of complete inactivation of lipase activity, T50 which represents the temperature at which the lipase activity was reduced by half and T100 designated the maximum temperature where lipase activity remained unaffected CH5183284 cost within 20 min of incubation. Figure Teicoplanin 3 Temperature-dependent heat inactivation of lipase LipA. Purified lipase LipA (18 ng/ml) from P. aeruginosa was incubated for 20 min in the absence (−○-) and in the presence of 1 mg/ml (−■-) bacterial alginate from P. aeruginosa SG81 shown in red, (−–) deacetylated bacterial alginate from P. aeruginosa SG81 shown in orange, (−♦-) bacterial alginate from P. aeruginosa FRD1 shown in dark blue, (−◊-) bacterial alginate from P. aeruginosa FRD1153 shown in bright blue. Results are shown as mean of three independent experiments with standard deviations. In summary, the protection effect of alginate occurred mainly at temperatures between 50°C and 80°C. The inactivation of lipase activity at 70°C was investigated in more detail over an increased incubation time (Figure 4). In general, similar results were obtained even over a prolonged incubation time of 60 min.

However, the original Schwartz equation is based on serum Cr determined by the Jaffe method. This equation may overestimate the GFR if serum Cr is determined by the enzymatic method. Therefore, serum Cr should be converted before adopting the Schwartz equation. To convert serum Cr measured by the enzymatic method to that measured

by the Jaffe method, Eq. 2 can BVD-523 be used. Equation 3 is the new Schwartz equation and is an updated equation used to calculate GFR utilizing the enzymatic method. However, the revised formula still overestimates GFR when applied to Japanese children. This may be due to differences in body mass and body height between Japanese and Western children. Recently, the Committee of Measures for CKD in children of the Japanese Society of Pediatric Staurosporine Nephrology established a new formula by measuring inulin clearance in Japanese children aged 2–11 years (Eq. 4, Table 12). Table 12 Constant k for the Schwartz formula Age Constant k (gender) 1 week Premature infants 0.33 (male and female) Term infants 0.45 (male and female) 2 weeks–1 year 0.45 (male and female) 2–12 years 0.55 (male and female)

13–21 years 0.70 (male) Urease 0.55 (female) 3. Reference serum creatinine   Although serum Cr is the most commonly used marker for kidney function, serum Cr is affected by factors other than GFR, principally Cr production, which is related to body size and muscle mass. This leads to considerable variability between children of different ages and a relatively wide range of serum Cr levels

in normal individuals. Therefore, the Committee of Measures for CKD in Children of the Japanese Society of Pediatric Nephrology established a normal reference value of serum Cr for see more healthy Japanese children in 2011 (Table 13). Table 13 Serum Cr distribution in healthy Japanese children (enzymatic method) Age 2.50 % 50.00 % 97.50 % 3–5 (months) 0.14 0.2 0.26 6–8 0.14 0.22 0.31 9–11 0.14 0.22 0.34 1 (year) 0.16 0.23 0.32 2 0.17 0.24 0.37 3 0.21 0.27 0.37 4 0.2 0.3 0.4 5 0.25 0.34 0.45 6 0.25 0.34 0.48 7 0.28 0.37 0.49 8 0.29 0.4 0.53 9 0.34 0.41 0.51 10 0.3 0.41 0.57 11 0.35 0.45 0.58 Age (years) Male Female 2.50 % 50.00 % 97.50 % 2.50 % 50.00 % 97.50 % 12 0.4 0.53 0.61 0.4 0.52 0.66 13 0.42 0.59 0.8 0.41 0.53 0.69 14 0.54 0.65 0.96 0.46 0.58 0.71 15 0.48 0.68 0.93 0.47 0.56 0.72 16 0.62 0.73 0.96 0.51 0.59 0.74 For children aged 2–11 years, the reference serum Cr level can be estimated using a simple equation (Eq. 5). For all children under 18 years of age, the individual serum Cr reference value can be estimated using a polynomial formula (Eq. 6).

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A, Kutilek APR-246 chemical structure S, Libanati C, McClung MR, Reid IR, Resch H, Siris E, Uebelhart D, Wang A, Weryha G, Cummings SR (2011) Effects of denosumab on bone turnover markers in postmenopausal osteoporosis. J Bone Miner Res 26:530–537PubMedCrossRef

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