J Bacteriol 1996, 178:175–183.PubMed 5. Mack D, Haeder M, Siemssen N, Laufs R: Association of biofilm production of coagulase-negative staphylococci with expression of a specific polysaccharide intercellular adhesion. J Infect Dis 1996, 174:881–884.PubMedCrossRef 6. Mack D, Nedelmann M, Krokotsch A, Schwarzkopf A, Heesemann

J, Laufs R: Characterization of Transposon Mutants of Biofilm-Producing Staphylococcus epidermidis Impaired in the Accumulative Phase of Biofilm Production: Genetic Identification of a Hexosamine-Containing Polysaccharide Intercellular Adhesin. Infect Immun 1994, 62:3244–3254.PubMed 7. Mack D, Siemssen N, Laufs R: Parallel selleck compound Induction of Glucose of Adherence and a Polysaccharide Antigen Specific for Plastic-Adherent Staphylococcus epidermidis: Evidence for Functional Relation to Intercellular Adhesion. Infect Immun 1992, 60:2048–2057.PubMed 8. Rupp M, Ulphani JS, Fey

PD, Mack D: Characterization of Staphylococcus epidermidis Polysaccharide Intercellular Adhesin/Hemagglutinin PI3K inhibitor in the Pathogenesis of Intravascular Catheter-Associated Infection in a Rat Model. Infect Immun 1999, 67:2656–2659.PubMed 9. Vuong C, Voyich JM, Fischer ER, Braughton KR, Whitney AR, DeLeon FR, Otto M: Polysaccharide intercellular adhesin (PIA) protects Staphylococcus epidermidis against major components of the human innate immune system. Cell Microbiol 2004, 6:269–275.PubMedCrossRef 10. Kristian SA, Birkenstock TA, Sauder U, Mack D, Götz F, Landmann R: Biofilm Selleck AZD4547 formation induces C3a release and protects Staphylococcus epidermidis from IgG and complement deposition and from neutrophil-dependent killing. J Infect Dis 2008, 197:1028–1035.PubMedCrossRef 11. Heilmann C, Schweitzer O, Gerke C, Vanittanakom N, Mack D, Götz F: Molecular

basis of intercellular adhesion in the biofilm-forming Staphylococcus epidermidis. Mol Microbiol 1996, 20:1083–1091.PubMedCrossRef 12. Heilmann C, Gerke , Perdreau-Remington click here F, Gotz F: Characterization of Tn917 insertion mutants of Staphylococcus epidermidis affected in biofilm formation. Infect Immun 1996, 64:277–282.PubMed 13. Gerke C, Kraft A, Suβmuth R, Schweitzer O, Gotz F: Characterization of the N-Acetylglucosaminyltransferase Activity Involved in the Biosynthesis of the Staphylococcus epidermidis Polysaccharide Intercellular Adhesin. J Biol Chem 1996, 273:18586–18593.CrossRef 14. Arvaniti A, Karamanos NK, Dimitracopoulos G, Anastassiou ED: Isolation and Characterization of a Novel 20-kDa Sulfated Polysaccharide from the Extracellular Slime Layer of Staphylococcus epidermidis. Arch Biochem Biophys 1994, 308:432–438.PubMedCrossRef 15.

If so, perhaps the muscle pump cleared this oedemata during the race, and perhaps clearing was aided by compression socks. Regarding the results concerning the decrease in the circumferences of both the thigh and the calf, we expected that the main areas of decrease would occur in the muscles AZD1480 chemical structure used most, meaning

in the lower leg and thigh muscles. Because the thigh has a larger skeletal muscle mass than the calf, it is likely that the change in the thigh muscle mass influenced the change in estimated skeletal muscle mass more than the change in calf muscle mass did. Another possible explanation could be that there actually would have been a correlation selleckchem between the decrease of the lower leg volume and the estimated skeletal muscle mass, but that this correlation was influenced due to a non-quantified change in tissue fluid in the lower leg. As we were using plethysmography for measuring the volumes of the whole limbs, we were not able to differentiate a change in volume between arm and hand or between lower leg and foot,

respectively. This could have influenced our results. Lund-Johansen et al.[14] measured the displaced water by weighing, which is a similar method to the plethysmography. These authors concluded Compound C solubility dmso that water displacement volumetry was a sensitive method for the measurement of leg volume. We therefore think that using plethysmography for measuring the leg volume is a sensitive method as well. Unfortunately, both methods have the limitation of not being able to differentiate between volume changes in the measured compartment or to differentiate between the volume changes of the body composition.

For example, if the volume of the lower leg decreases due to a depletion of intramyocellular stored energy while the same amount of volume increases due to oedemata occurring in the skeletal DOK2 muscle mass or in the adipose subcutaneous tissue, we could not measure any volume change using plethysmography. In previous studies, it was shown that oedemata did not develop immediately with the exercise or the race but shortly afterwards. Knechtle et al.[8] measured the highest total body water one day after a Triple Iron ultra-triathlon, Williams et al.[1] described a peak water retention on day 5 of consecutive hill-walking and Milledge et al.[2] measured the largest gain in the leg volumes one day after five consecutive days of hill-walking. There is inactive time between exercise bouts, no muscle pump, and therefore the possibility for swelling to build. Nor is there any mechanism to decrease swelling on subsequent days. Potential correlation between oedemata and renal function? Another interesting finding was that the change in the thicknesses of adipose subcutaneous tissue at medial border of the tibia was significantly and positively associated with the change in creatinine clearance.

Thus, we speculate that the urease of H. influenzae facilitates nitrogen assimilation in the nutritionally limited environment of the human airways and the middle ear space. Two indirect lines of evidence have suggested that H. influenzae

expresses urease during human infection. Mason et al [14] showed that urease H is expressed during infection of the middle ear in chinchillas and Qu et al [13] showed that urease C was expressed in markedly increased abundance during growth in pooled human sputum. The present study advances those observations by showing directly that H. influenzae expresses urease during airway infection in adults who experienced exacerbations of COPD. Paired pre and post infection serum samples were subjected to ELISA with purified recombinant urease C to characterize the Trichostatin A research buy antibody response to urease following infection. Because EPZ004777 order the pre infection serum samples were collected one month prior to acquisition of the infecting strain of H. influenzae, an increase in the level of antibody to urease indicates the development of new antibodies following infection.

All serum samples had detectable levels of antibody to urease and 7 of 18 patients developed significantly increased levels following infection compared to their own pre infection levels (Figure selleck kinase inhibitor 9). This frequency of antibody response following bacterial infection is typical as heterogeneity in immune responses to bacterial antigens among individuals is a hallmark of COPD [47, 48]. Note also that recombinant purified urease C was used in the ELISA and this protein is only one of 3 proteins that comprise the urease complex; thus, a urease C-based ELISA may underestimate the frequency of new antibody responses to urease following

infection. These results indicate MycoClean Mycoplasma Removal Kit that H. influenzae expresses urease during exacerbations of COPD and that urease is a target of human antibody responses. An important result from the present study is the observation that urease functions to mediate survival of H. influenzae in an acid environment. Urease mediates survival in low pH as a virulence mechanism in other bacteria, notably H. pylori which must survive in the stomach. Other selected respiratory pathogens express urease but the role of urease in pathogenesis of respiratory tract infection is unclear [49, 50]. Microenvironments in the human respiratory tract are likely low pH, consistent with the speculation that the high level of expression of urease in the respiratory tract mediates survival in acid microenvironments. Furthermore, H. influenzae is now known to invade and persist in respiratory epithelial cells and macrophages, suggesting that withstanding lower pH in intracellular compartments may be a virulence mechanism [51–53]. Conclusions The present study demonstrates that 1) The ureA-ureH gene cluster of H.

PubMed 14. Smith GL, Bunker GB, Dinneen MD: Fournier’s gangrene. BJU 1998, 81:347–355.PubMedCrossRef 15. MK-1775 Fournier JA: Gangrene foudroyante de la verge. Medecin Practique 1883, 4:589–597. 16. Unalp HR, Kamer E, Derici H, Atahan K, Balci U, Demirdoven C, Nazli O, Onal MA: Fournier’s gangrene: Evaluation of 68 patients and analysis of prognostic variables. J Postgrad Med 2008, 54:102–105.PubMedCrossRef 17. Tuncel A, Aydin O, Tekdogan U: Fournier’s Gangrene: Three years of experience with 20 patients and validity of the Fournier’s gangrene severity index score. Eur Urol 2006, 50:838–843.PubMedCrossRef 18. Czymek R, Frank P, Limmer S, Schmidt A, Jungbluth T, Roblick U, Bürk C,

Bruch HP, Kujath P: Fournier’s gangrene: is the NF-��B inhibitor female gender a risk factor? Langenbecks Arch Surg 2010, 395:173–180.PubMedCrossRef 19. Malik AM, Sheikh S, Pathan R, Khan A, Sheikh U: The spectrum of presentation and management of Fournier’s gangrene-An Experience Selleckchem Compound C of 73 Cases. J Pak Med Assoc 2010, 60:617–619.PubMed 20. Sallami S, Maalla R, Gammoudi A, Ben Jdidia G, Tarhouni L, Horchani A: Fournier’s Gangrene: What are the prognostic factors? Our experience with 40 patients. La Tunisie Medicale 2012, 90:708–714.PubMed 21. Yilmazlar T, Ozturk E, Ozguc H: Fournier’s Gangrene: An analysis of 80 patients and a novel scoring system. Tech Coloproctol 2010, 14:217–223.PubMedCrossRef

22. Ruiz-Tovar J, Córdoba L, Devesa JM: Prognostic Factors in Fournier Gangrene. Asian J Surg 2012, 35:37–41.PubMedCrossRef 23. García A, Martín J, Vaquero A, Sánchez T, de Tomás J, Lago J, Turégano F: Fournier’s gangrene: analysis of prognostic variables in 34 patients. European Journal of Trauma and Emergency Surgery 2011, 37:141–145.CrossRef 24. Jarboui S, Jarraya H, Daldoul S, Zaouche A: Étude clinique et thérapeutique et analyse pronostique des gangrènes du périnée. Presse Med 2008, 37:760–766.PubMedCrossRef

25. Dahm P, Roland FH, Vaslef SN, Moon RE, Price DT, Georgiade GS, Vieweg J: Outcome analysis in patients with primary necrotizing fasciitis of the male genitalia. Urology 2000, PRKACG 56:31–35.PubMedCrossRef 26. Nisbet AA, Thompson IM: Impact of diabetes mellitus on the presentation and outcomes of Fournier’s gangrene. Urology 2002, 60:775–779.PubMedCrossRef 27. Laor E, Palmer LS, Tolia BM, Reid RE, Winter HI: Outcome prediction in patients with Fournier’s gangrene. J Urol 1995, 154:89–92.PubMedCrossRef 28. Martinschek A, Evers B, Lampl L, Gerngroß H, Schmidt R, Sparwasser C: Prognostic aspects, survival rate, and predisposing risk factors in patients with Fournier’s gangrene and necrotizing soft tissue infections: evaluation of clinical outcome of 55 patients. Urol Int 2012, 89:173–179.PubMedCrossRef 29. Ersoz F, Sari S, Arikan S, Altiok M, Bektas H, Adas G, Poyraz B, Ozcan O: Factors affecting mortality in Fournier’s gangrene: experience with fifty-two patients. Singapore Med J 2012, 53:537–540.PubMed 30.

The antibiotics were serially diluted in 1 mL of M79 medium at concentrations from 256 μg/mL to 0.5 μg/mL. An overnight culture of A. amazonense was diluted to 4 × 104 cells/mL. One milliliter of this dilution was added to one milliliter of M79 medium containing the appropriate antibiotic concentration. The cells were cultivated in a rotary shaker at 150 rpm for 40 h at 35°C. Conjugation Conjugation was basically carried out as described by Clerico et al. (2007) [42]. However, some modifications were made as follows: overnight cultures of A. amazonense Y2 (receptor), E. coli XL1-Blue containing the plasmid pRK2013 (helper), and E. coli XL1-Blue containing the appropriate plasmid (donor) were used.

Approximately 1 mL of the A. amazonense culture with an OD600 = 2 (1.3 × 109 cfu/ml) was mixed with 1 mL of each helper and donor cultures with an OD600 = 0.2 (2 × 108 cfu/mL) check details (ratio 10:1:1), unless stated otherwise. This mixture was harvested by centrifugation at 6000 g for 2 min and then resuspended in 100 μL of MLB medium (LB and M79 mixture at a proportion of 8:2), and this volume was then spotted onto MLB agar and incubated for 20 h at 35°C. Following this, the cell mass

was resuspended in 200 μL of M79 medium and plated on M79 medium containing the appropriate antibiotic. Electroporation The preparation of cells was based on the protocol described by Schultheiss and Schüler (2003) [27]. A 3 mL PRN1371 mw overnight culture of A. amazonense was inoculated in 250 mL of M79 and the cells were cultivated to an OD600 of ~0.12 (early-log growth phase), unless stated otherwise. From this point, all manipulations were conducted on ice. The cells were incubated in ice for 30 min and then harvested by Neratinib supplier centrifugation at 5000 g for 20 min at 10°C. The cells were resuspended in 100 mL of electroporation buffer (pH 6.5 HEPES 1 mM, MgCl2 1 mM, and sucrose 200 mM) and again harvested by centrifugation (20 min at 5000 g). Subsequently, the cells were resuspended in 40 mL of electroporation buffer and again harvested by centrifugation. At the end, the cells were resuspended

in 250 μL of electroporation buffer (final concentration of ~1010 cfu/mL), distributed in aliquots of 40 μL, and frozen in liquid nitrogen. Cell electroporation was carried out as follows: the 40 μL aliquot was mixed with 50 ng of the pHRGFPGUS vector and electroporated Cell Cycle inhibitor through a Gene Pulser apparatus (Bio-Rad Laboratories Inc.) with 12.5 kV/cm, 25 μF and 200 Ω, unless stated otherwise. After electrical discharge, the cells were resuspended in 500 μL of M79 medium and incubated at 35°C for 3 h in a rotary shaker at 150 rpm. Subsequently, the cells were plated on solid M79 medium containing 20 μg/mL of kanamycin and incubated for 2 days at 35°C. Gene mutagenesis Site-directed mutagenesis was based on a protocol described by Eggeling and Reyes (2005) [43].

PTS group translocators, like ABC transporters, are usually high affinity systems that recognize their sugar substrates with micromolar or sub-micromolar affinities. Since they use phosphoenolpyruvate to energize uptake, the same arguments presented for ABC transporters apply. Monocarboxylates (3.6% – 23 total) are transported by 15 secondary carriers and 11 primary active transporters. Di- & tricarboxylates and

aromatic compounds are transported solely by secondary carriers while noncarboxylic organoanions are mostly transported by secondary carriers. In summary, sugars are transported primarily by ATP-driven porters, while organic anionic compounds are transported primarily by pmf-driven carriers. This observation is in agreement with the primary energy source generated by the metabolism of these compounds (ATP from sugars; the pmf from organic acids). Amino acids & their derivatives are transported primarily by secondary carriers although peptides are taken VS-4718 cost up almost exclusively by ABC systems. Transporters for amino acids and conjugates (9% – 56 total) include secondary carriers

(39 see more proteins), primary active transporters (16 proteins), and a single channel. Amines, amides, polyamines & organocations (2.4% – 15 total) were found to be transported by both primary active transporters (5 proteins) and secondary carriers (7 proteins). They are also transported by two amino sugar OICR-9429 supplier uptake group translocators (both TC# 4.A.1.1.5) and a channel protein (TC# 1.A.11.1.3). With the exception of one secondary carrier (TC# 2.A.17.1.1), almost all peptides (3.8% – 21 total) are taken up or expelled by primary active transporters (20 proteins). Considered collectively, nitrogenous compounds are thus transported roughly equally by primary and secondary carriers. Vitamins and especially iron siderophore complexes are primarily

taken up via ABC-type active transporters. Specifically, vitamins & vitamin or cofactor precursors are taken up by primary active transporters (5 proteins), secondary carriers (3 proteins) and a single group translocator. Transporters for siderophores and siderophore-Fe find more complexes (29 total) are mostly primary active transporters (21 proteins), with fewer secondary carriers (8 proteins). This fact probably reflects the need for high affinity recognition due to the low concentrations of these substances in the external environment. Transport of drugs and other hydrophobic substances occurs primarily by secondary pumps. Systems for multiple drugs (8.7% – 56 total) are exported via secondary carriers (36 proteins) and primary active transporters (20 proteins), but almost all of the specific drug exporters (62 total) are secondary carriers (58 proteins), with only four exceptional primary active transporters. By contrast, of the 8 pigment exporters identified [26, 27], 7 proved to be primary carriers. All other systems specific for hydrophobic substances are primary active transporters.

As we explore the mechanism of montmorillonite catalysis and the properties of the RNA oligomers formed, we find that not all montmorillonites are catalysts. Those having a lower layer charge allow the activated monomers to intercalate the montmorillonite platelets where catalysis occurs. Those with a higher

layer charge have a greater concentration of cations in the interlayer preventing monomers from intercalating between the montmorillonite platelets. The montmorillonites that are catalysts all have similar elemental compositions. We are GDC 0032 solubility dmso currently investigating if the RNA oligomers formed by montmorillonite are catalysts. Oligomers of RNA are prepared from mixtures of 2, 3 or 4 activated RNA monomers. They are then passed through an affinity column in Pevonedistat nmr which an agarose gel has an attached spacer arm with the target molecule (amino acids, nucleotides etc.) attached to its end. Those RNA oligomers that bind to the target molecule will be isolated and tested for their ability to catalyze reactions of the target molecule. If catalysis is observed this TGF-beta inhibitor finding will be consistent with the RNA world hypothesis that these RNAs are catalysts. E-mail: ferrij@rpi.​edu Not to Put the Cart Before the Horse A.

G. Cairns-Smith Chemistry Department, Glasgow University, UK Darwin fully acknowledged the difficulties in seeing how such a thing as an eye might have evolved through natural selection (Darwin 1859, Chapter 6), but he knew of many lesser examples that could clearly have arisen that way.

If the detailed, well adapted, shape of a bird’s beak could have arisen through natural selection without the need for a prior creator, then Nature can indeed act as if it were an engineer, producing what seem to be purpose-built structures, and giving an impression of foresight. But, really, no mysterious view of the future is required. What is absolutely required for nature’s engineer to get to work is remarkable all the same: it is a kind of memory of what succeeded in the past. So this is the question that should be the first focus of Staurosporine in vivo our attention: What are the simplest genetic memories that we can imagine working in a primitive geochemical milieu? The RNA world idea has been a great inspiration, but this system is already too sophisticated and too far from ordinary geochemistry to be a likely beginner in the evolution game. I have suggested that the mineral world provides us with several candidates for more primitive genetic materials (Cairns-Smith 2005, 2008 and references therein). I will argue against the usual approach to the puzzle of the origin of life, which looks for ways in which the present molecules of life might have arisen as a prelude to a Darwinian evolution. I think that this puts the cart before the horse.

As the temperature increases, the overall learn more resistance of the WO3 nanowire will decrease

correspondingly, which is consistent with that of a typical semiconductor. On the other hand, the WO3 nanowire will exhibit hysteretic resistance switching though the bias sweep range is https://www.selleckchem.com/products/prt062607-p505-15-hcl.html less than 1 V. The electrical transport properties of WO3 are known to be governed by the hopping conduction mechanism, and the electrons localized at the oxygen vacancies are the major carriers [1]. Theoretical calculations and experimental results indicate that the electrical transport and optical properties of WO3−x films depend on the levels of oxygen vacancies: films with x > 0.2 are metallic and conductive, and those with x < 0.167 are transparent and resistive [17]. The oxygen vacancies act as +2-charged dopants and will drift when the electric field strength is strong enough, which will modulate the concentration

distribution of oxygen vacancies and then the electrical transport properties. At room temperature, when bias voltage less than 1 V is applied to the two electrodes with a separation of 1 μm, the strongest electric field in the WO3 nanowire will be less than 106 V/m, and the drift of oxygen vacancies is negligible. At the moment, WO3 nanowires exhibit resistive characteristics, and the I V curves are perfectly linear and symmetric. The drift of oxygen vacancies can be enhanced evidently by increasing the strength of electric field or the temperature, which will result in KU-57788 research buy a change in the concentration of oxygen vacancies along the axial direction and then the resistance of the WO3 nanowire. The resistance of WO3 nanowire keeps at a minimum value when oxygen vacancies distributes

uniformly along the axial direction. When the bias voltage is swept from 0 to V max (−V max) and then back to 0, the drift Vorinostat nmr of oxygen vacancies results in departure from the uniform distribution, which will lead to device switching gradually to high resistance state. When the bias voltage is swept subsequently from 0 to −V max (V max) and then back to 0, the drift of oxygen vacancies restores the uniform distribution, which will lead to device switching gradually to low resistance state. Therefore, the critical electric field for oxygen vacancy drifting in WO3 nanowire is one order of magnitude less than that in its granular film [28], which might be attributed to its nanoscale diameter and single crystalline structure. Figure 2 Log-scale and linear-scale (inset) I – V curves recorded for an individual WO 3 at different temperatures. Another important characteristic of these I-V curves in Figure 2 is an increase in the asymmetry between positive and negative bias voltages with increasing temperature, which might be attributed to the asymmetry in the two ohmic contacts between WO3 nanowire and electrodes. Figure 3a shows the typical I-V curves recorded at different temperature in vacuum for the WO3 nanowire device with obviously asymmetric ohmic contacts.

Numbers at branch-points are percentages of 1000 bootstrap resamplings

that support the topology of the tree. Sequencing was carried out on the fliC gene of sixteen randomly selected isolates of R. pickettii, and the type strain of R. insidiosa. The phylogenetic analysis of the fliC gene can be seen in Figure 2b, with the isolates divided into two branches with B. cepacia as an out-group. The isolates identified as R. insidiosa in-group two grouped together with groups three BIBW2992 cell line and four. These however were not supported by high bootstrapping values. Group 1 is made up of R. pickettii isolates from clinical and environmental sources with 97-100% similarity to the R. pickettii type strain. Group 2 is made up of R. insidiosa with 85% similarity to the R. pickettii type strain; Group 3 is made up of both R. insidiosa and R. pickettii with 86-87% similarity to the R. pickettii type strain and Group 4 is made up of the available sequenced R. pickettii strains with 87% similarity to the R. pickettii type strain. The division of the groups did not correlate to clinical or environmental association or on their isolation location. These Ricolinostat solubility dmso results indicate that there see more is variation in

the flagellin gene of R. pickettii. RAPD PCR results and analysis RAPD analysis was carried out using four different primers, three of which (P3, P15 and M13) have been shown to discriminate between selleckchem closely related strains of Ralstonia spp. including R. mannitolilytica and Cupriavidus pauculus [Ralstonia paucula] [47, 48]. The reproducibility of the RAPD method was tested by repeating the RAPD assays at least three times for each primer used (data not shown). The results revealed that apart from some variations in the band intensity, no significant differences were observed between the profiles

obtained, confirming the reproducibility of the method. Fifty-nine isolates of R. pickettii and R. insidiosa were characterised by RAPD analysis using all four primers and all isolates were placed into genotypes (Table 3). Percent similarities based on the Pearson correlation coefficients and clustering by the UPGMA method for these isolates using the OPA03U primer is presented in Figure 3a. Dendograms for the other primers (P3, P15 and M13) are presented in Additional File 2, Figure S1, S2 and S3. Fragments ranged from approximately 100 to 1800 bp for all primers. Clusters were distinguished at a similarity cut-off level of 80%. No major differentiation between the clinical, industrial, laboratory purified water and type strains could be observed, as these all fell into separate groups (Table 3) with each primer. For each of the primers there were a number of groups, with M13 there were twenty-one groups, OPA3OU there were 15 groups, P3 there were twenty-five groups and with primer P15 there were twenty-one groups.

J Clin Endocrinol Metab 86:192–199PubMedCrossRef 12. Van Pottelbergh I, Goemaere S, Kaufman JM (2003) Bioavailable estradiol and an aromatase gene polymorphism are determinants of bone mineral density changes in men over 70 years of age. J Clin Endocrinol Metab 88:3075–3081PubMedCrossRef 13. Fink HA, Ewing SK, Ensrud KE, Barrett-Connor E, Taylor BC, Cauley JA, Orwoll ES (2006) Association of testosterone and estradiol deficiency with osteoporosis

and rapid bone loss in older men. J Clin Endocrinol Metab 91:3908–3915PubMedCrossRef 14. Khosla S, Melton LJ 3rd, Robb RA, Camp JJ, Atkinson EJ, Oberg AL, Rouleau PA, Riggs BL (2005) Relationship of volumetric BMD and structural parameters at different skeletal sites to sex steroid levels in men.

J Bone Miner Res 20:730–740PubMedCrossRef 15. Szulc P, Uusi-Rasi K, Claustrat B, Marchand F, Beck TJ, Delmas PD (2004) Role of sex steroids in the regulation of bone find more morphology in men. The MINOS study. Osteoporos Int 15:909–917PubMedCrossRef 16. Lauretani F, Bandinelli S, Russo CR, Maggio M, Di Iorio A, Cherubini A, Maggio D, Ceda GP, Valenti G, Guralnik JM, Ferrucci L (2006) Correlates of bone quality in older persons. Bone 39:915–921PubMedCrossRef 17. Bjornerem A, Ahmed LA, Joakimsen RM, Berntsen GK, Fonnebo V, Jorgensen L, Oian P, Seeman E, Straume B (2007) GF120918 mw A prospective study of sex steroids, sex hormone-binding globulin, and non-vertebral fractures in women and men: the Tromso Study. Eur J Endocrinol 157:119–125PubMedCrossRef 18. Bjornerem A, Emaus N, Berntsen GK, Joakimsen RM, Fonnebo V, Wilsgaard T, Oian P, Seeman E, Straume B (2007) Circulating sex steroids, sex hormone-binding globulin, and longitudinal changes in forearm bone mineral density in postmenopausal women and men: the tromso study. Calcif Tissue Int 81:65–72PubMedCrossRef 19. Goderie-Plomp HW, van der Klift M, de Ronde W, Hofman A, de Jong FH, Pols HAP (2004) Endogenous sex hormones, sex hormone-binding globulin, and the risk of incident vertebral fractures in elderly men and women: the Rotterdam study. J Clin Endocrinol Metab 89:3261–3269PubMedCrossRef many 20. Lee DM, O’Neill TW, Pye

SR, Silman AJ, Finn JD, Pendleton N, Tajar A, PCI32765 Bartfai G, Casanueva F, Forti G, Giwercman A, Huhtaniemi IT, Kula K, Punab M, Boonen S, Vanderschueren D, Wu FC (2009) The European Male Ageing Study (EMAS): design, methods and recruitment. Int J Androl 32:11–24PubMedCrossRef 21. Augat P, Reeb H, Claes L (1996) Prediction of fracture load at different skeletal sites by geometric properties of the cortical shell. J Bone Miner Res 11:1356–1363PubMedCrossRef 22. Schiessl H, Ferretti J, Tysarczyk-Niemeyer G, Willnecker J (1996) Noninvasive bone strength index as analyzed by peripheral quantitative computed tomography (pQCT). In: Schoenau E (ed) Paediatric osteology: new developments in diagnostics and therapy. Elsevier, Amsterdam, pp 141–146 23.