Microbiol 2010, 156(Pt 2):555–560 CrossRef 10 Calix JJ, Nahm MH:

Microbiol 2010, 156(Pt 2):555–560.CrossRef 10. Calix JJ, Nahm MH: A new pneumococcal serotype, 11E, has a variably inactivated wcjE gene. J Infect Dis 2010, 202(1):29–38.PubMedCentralBIX 1294 PubMedCrossRef 11. Calix JJ, Porambo RJ, Brady AM, Larson TR, Yother J, Abeygunwardana C, Nahm MH: Biochemical, genetic, and serological characterization of two capsule subtypes among Streptococcus pneumoniae Serotype 20 strains: discovery of a new pneumococcal serotype. J Biol Chem

2012, 287(33):27885–27894.PubMedCentralPubMedCrossRef 12. Kolkman MA, van der Zeijst BA, Nuijten PJ: Diversity of capsular polysaccharide synthesis gene clusters in Streptococcus pneumoniae . J Biochem 1998, 123(5):937–945.PubMedCrossRef 13. Garcia E, Llull D, Munoz R, Mollerach M, Lopez R: Current trends in capsular polysaccharide biosynthesis of Streptococcus pneumoniae . Res Microbiol 2000, 151(6):429–435.PubMedCrossRef Smad inhibitor 14. Morona JK, Paton JC, Miller DC, Morona R: Tyrosine phosphorylation of CpsD negatively regulates capsular polysaccharide PF477736 biosynthesis in Streptococcus pneumoniae . Mol Microbiol 2000, 35(6):1431–1442.PubMedCrossRef 15. Morona JK, Miller DC, Morona R, Paton JC: The effect that mutations in the conserved capsular polysaccharide

biosynthesis genes cpsA , cpsB , and cpsD have on virulence of Streptococcus pneumoniae . J Infect Dis 2004, 189(10):1905–1913.PubMedCrossRef 16. van der Windt D, Bootsma HJ, Burghout P, van der Gaast-de Jongh CE, Hermans PW, van der Flier M: Nonencapsulated Streptococcus pneumoniae resists extracellular human neutrophil elastase- and cathepsin G-mediated killing. FEMS Immunol Med Microbiol 2012, 66(3):445–448.PubMedCrossRef

17. Martin M, Turco JH, Zegans ME, Facklam RR, Sodha S, Elliott JA, Pryor JH, Beall B, Erdman DD, Baumgartner YY, Sanchez PA, Schwartzman JD, Montero J, Schuchat A, Whitney CG: An outbreak of 3-mercaptopyruvate sulfurtransferase conjunctivitis due to atypical Streptococcus pneumoniae . N Engl J Med 2003, 348(12):1112–1121.PubMedCrossRef 18. Crum NF, Barrozo CP, Chapman FA, Ryan MA, Russell KL: An outbreak of conjunctivitis due to a novel unencapsulated Streptococcus pneumoniae among military trainees. Clin Infect Dis 2004, 39(8):1148–1154.PubMedCrossRef 19. Porat N, Greenberg D, Givon-Lavi N, Shuval DS, Trefler R, Segev O, Hanage WP, Dagan R: The important role of nontypable Streptococcus pneumoniae international clones in acute conjunctivitis. J Infect Dis 2006, 194(5):689–696.PubMedCrossRef 20. Beiter K, Wartha F, Hurwitz R, Normark S, Zychlinsky A, Henriques-Normark B: The capsule sensitizes Streptococcus pneumoniae to alpha-defensins human neutrophil proteins 1 to 3. Infect Immun 2008, 76(8):3710–3716.PubMedCentralPubMedCrossRef 21. Nelson AL, Roche AM, Gould JM, Chim K, Ratner AJ, Weiser JN: Capsule enhances pneumococcal colonization by limiting mucus-mediated clearance.

The high prevalence of

The high prevalence of accidents involving road traffic has also been reported by several national and international authors [15, 22–25]. Montenegro et al [27], studying mortality among motorcyclists in the Federal District (Brazil), found that over 70% of deaths occurred in hospitals. Furthermore they conclude that despite the severity of injuries, it is possible that the availability of emergency services and APH explain the lower proportion of deaths on public roads when compared to countries with disorganized public health systems.

Marín-León et al [28], studying the trend of traffic accidents in Campinas (SP-Brazil), Akt molecular weight found an increase of 241% in the fleet of motorcycles in little more than a decade, representing almost 50% of all fatal accidents on public roads in 2008. In the present

study motorcycles were involved in 32.8% of injury causes, rising to 56.7% when only road traffic accidents are considered, corroborating the above authors to conclude that multi-institutional actions are necessary to prioritize the prevention of motorcycle accidents. A recently published study shows that violence and road traffic accidents account for almost two thirds of deaths of all trauma injuries [2]. In Brazil, homicide is listed as the most common cause of death, closely GW2580 mw followed by road traffic accidents (36.4% and 29.3% respectively, in 2007). Mascarenhas et al [29] and Gawryszewski et al [30], analyzing emergency department visits buy Nec-1s due to traumatic Endonuclease injury in the Sentinel Services of Surveillance of Violence and Accidents system (VIVA), report that 10.4% of patient visits are motivated by violence, which affects more men than women. They also report a fact that draws attention, which is the means of transport used to get to the hospital: 25.2% of patients used

private vehicles, and only 19.9% used a SAMU vehicle. Also in relation to causes of injury, this study observed that 25.8% of patients were victims of falls, mostly being attended by SAMU. It is a fact that falls, and the resulting injuries, are more common among the elderly. Mello and Moyses [31], studying violence and accidents among the elderly, found in Curitiba (PR-Brazil) a prevalence of 22.5% of calls outs involving elderly patients, and that of these, 3.6% were victims of external causes. Analyzing the pre-hospital transport systems, statistical differences were obtained for all the calculated times, with the CB showing shorter times in all the measurements (p<0.05). In fact, according to the working philosophy of this institution, these findings are within the expected range. The CB is heavily influenced by the North American system, which operates according to a working proposal of minimal intervention and maximum speed of transport.

2 ± 18 1 138 6 ± 19 8 Data reported are Mean ± SEM * = significan

2 ± 18.1 138.6 ± 19.8 Data reported are Mean ± SEM * = significant main-effect for time (p < 0.05) # = significant time-effect between Pre-ITD and Post4 Table 5 Performance Tests   Treatment Period Performance Test CHO CM T-Drill (s) 9.09 ± 0.13 9.06 ± 0.16 Vertical Jump (inches) 26.7 ± 1.0 26.7 ± 1.0 Data reported are Mean ± SEM Discussion Training programs for competitive soccer players include activities of varying intensities, which have been shown to deplete muscle glycogen stores [25, 26]. In addition, plyometric

exercises such as vertical jumping, which are a common component of soccer training, have been associated with increased muscle soreness, elevated blood CK levels and impaired performance in subsequent exercise [27]. Thus, the utilization of post-exercise nutrition interventions that influence these variables could potentially affect recovery in soccer players. The

purpose SN-38 of this investigation was to assess the efficacy of CM as a post-exercise recovery beverage in soccer players, compared to a carbohydrate-only beverage. The recovery drinks were matched in total caloric content (504 kcal/serving), and both beverages contained carbohydrate in amounts that approached (CM: 1.1 g/kg) or exceeded (~CHO: 1.5 g/kg) levels associated with optimal post-exercise glycogen repletion [34, 35]. Although few studies have investigated the specific effects of CM on post-exercise recovery, our findings can also be compared with studies selleck chemicals llc investigating CHO+Pro recovery beverages, which contain carbohydrate and protein in similar proportions selleck kinase inhibitor to CM. Overall, the isocaloric CM and CHO supplements provided similar effects on markers of post-exercise recovery over the four-day period of ITD. No significant treatment*time interactions were observed for muscle soreness, ratings of energy/fatigue and muscle function (MVC). Similarly, AZD9291 order there were no treatment effects on serum Mb. However, serum CK levels were significantly lower following four days of ITD with CM supplementation versus CHO supplementation. Numerous studies of CHO+Pro beverages have reported attenuated post-exercise

plasma/serum CK levels after heavy endurance or resistance exercise [4, 5, 7–10], though this finding has not be observed in all studies [11, 12]. The reduced CK levels observed in this investigation is also consistent with Cade et al. [24] and Luden et al. [6], who reported lower plasma CK levels with CHO+Pro ingestion over the course of multiple days of training in free-living swimmers and runners, respectively. Our findings similarly suggest that CM may attenuate blood CK levels in athletes performing heavy soccer training. Plasma/serum CK is often used as a broad indicator of muscle damage. However, CK levels can be poorly correlated with direct measures of muscle damage or muscle function [36, 37]. Thus, the practical significance of modestly lower serum CK levels (~115 U/L) with CM is not clear.

New Zealand Plant Protection 2002, 55:150–153 31 Obanor F, Will

New Zealand Plant Protection 2002, 55:150–153. 31. Obanor F, Williamson K, Mundy D, Wood P, Walter M: Optimisation Chk inhibitor of PTA-ELISA detection and quantification of Botrytis cinerea infections

in grapes. New Zealand Plant Protection 2004, 57:130–137. 32. Ricker R, Marois J, Dlott R, Morrison J: Immunodetection and quantification of Botrytis cinerea on harvested wine grapes. Phytopathology 1991, 81:404–411.CrossRef 33. González C, Noda J, Espino J, Brito N: Drill-assisted genomic DNA extraction from Botrytis cinerea . Biotechnol Lett 2008, 30:1989–1992.PubMedCrossRef 34. Muñoz C, Gómez Talquenca S, Oriolani E, Arias F: Identificación rápida de distintas razas de Botrytis cinerea en cultivos de vid. Enologia 2008, 6:5–7. 35. Giraud T, Dominique F, Levis C, Leroux P, Brygoo Y: RFLP Markers show genetic recombination in Botrytinia Fuckeliana ( Botrytis cinerea ) and transposable element reveal two sympatric

species. Mol Biol Evol 1997, 11:1177–1185. 36. Giraud T, Fortini D, Levis C, Lamarque C, Leroux P, Lo Buglio K, Brygoo Y: Two sibling species of the Botrytis cinerea complex, transposa and vacuma , are found in sympatry on numerous host plants. Phytopathology 1999, 89:967–973.PubMedCrossRef 37. Fernández-Baldo MGCD0103 molecular weight M, Messina GA, Sanz MI, Raba J: Microfluidic immunosensor with micro magnetic beads coupled to Carbon-based Screen-Printed Electrodes

(SPCEs) for determination of Botrytis cinerea in tissue of fruits. J Agric Food Chem 2010, 58:11201–11206.CrossRef Authors’ contributions MFB participated in the design of the study, performed experiments and drafted the manuscript. JF carried out the molecular 17-DMAG (Alvespimycin) HCl genetic studies. SP and GM contributed to coordinate the study. ES helped in microbiological assays and in the obtention of antigen. JR helped to draft the manuscript and critically revised the manuscript. MSF participated in the study conception and coordination, provided guidance during all parts of the work, and helped to draft the manuscript. All authors read and approved the final version of the manuscript.”
“Background Acquisition of iron is essential for growth of most bacteria. However, due to insolubility at neutral pH the bioavailability of iron is extremely low in most natural environments. To circumvent this problem many bacteria respond to iron starvation by synthesizing high affinity https://www.selleckchem.com/products/ly3023414.html iron-chelating molecules known as siderophores. These siderophores are secreted into the extra-cellular environment where they bind ferric iron and are then actively transported back into the cell via specific ferric-siderophore receptors [1]. Siderophores play a prominent role in the biology of fluorescent pseudomonads, a genus renowned for occupying a very wide range of environmental niches.

Nat Rev Drug Discov 2008, 7:21–39 CrossRef 8 Steven PS: Recent a

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S, Randolph TW, Carpenter JF: Physical stability of proteins in aqueous solution: mechanism and driving forces in nonnative protein aggregation. Pharm Res 2003, 20:1325–1336.CrossRef Ilomastat 12. Wang W: Instability, stabilization,

and formulation of liquid protein pharmaceuticals. Int J Pharm 1999, 185:129–188.CrossRef 13. Fu K, Klibanoy AM, Langer R: Protein stability Temsirolimus solubility dmso in controlled-release systems. Nat Biotechol 2000, 18:24–25.CrossRef 14. Yuan WE, Wu F, Geng Y, Jin T: An effective approach to prepare uniform protein–Zn2+ nanoparticles under mild conditions. Nanotechnology 2007, 18:145601–145608.CrossRef 15. Yuan WE, Wu F, Geng Y, Xu SL, Jin T: Preparation of dextran glassy particles through freezing-induced phase separation. Int J Pharm 2007, 339:76–83.CrossRef 16. Sah H: Protein behavior at the water/methylene chloride interface. J Pharm Sci 1999, 88:1320–1325.CrossRef 17. Sah H: Protein instability toward organic solvent/water emulsification: implications for protein microencapsulation into microspheres. PDA J Pharm Sci Technol 1999, 53:3–10. 18. Huub S, Nicole C: Immunogenicity of recombinant human proteins: causes and consequences. J Neurol 2004, 251:1114–1119. 19. Eun SL, Min JK, Hyeok L, Jung JK: Stabilization of protein encapsulated in poly(lactide- co -glycolide) PAK6 microspheres by novel viscous S/W/O/W method. Int J Pharm 2007, 331:27–37.CrossRef 20. Brian C, Steven B, Jame AW: Zinc mediation of the binding of human growth hormone to the human prolactin receptor. Science 1990, 250:1709–1712.CrossRef 21. Johnson OL, Cleland JL, Lee HJ, Charnis M, Duenas E, Jaworowicz

W: A month-long effect from a single injection of microencapsulated human growth hormone. Nat Med 1996, 2:795.CrossRef 22. Brodbeck KJ, Pushpala S, McHugh AJ: Sustained release of human growth hormone from PLGA solution Talazoparib depots. Pharm Res 1999, 16:1825–1829.CrossRef 23. Andreas J, Annice M, Jan A, Linda S, Stephen MS: A new sustained-release preparation of human growth hormone and its pharmacokinetic, pharmacodynamic and safety profile. Clin Endocrinol 2005, 62:623–627.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions FW performed the experiment. LMW and WEY designed the experiments and wrote the manuscript. JS participated in the measurements. ZHZ and TJ provided useful suggestions.

Cardiol Rev 17(2):83–97CrossRef Ertel KA, Koenen KC, Berkman LF (

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105:73–83CrossRef Harbour R, Miller J (2001) A new system for grading recommendations in evidence based guidelines. BMJ 323(7308):334–336CrossRef Hemingway H, Marmot M (1999) Clinical Evidence: Psychosocial factors in the etiology and prognosis of coronary heart disease: systematic review of YH25448 mouse prospective cohort studies. West J Med 171(5–6):342–350 Hibbard JH, Pope CR (1993) The quality of social roles as predictors of morbidity and mortality. Soc Sci

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1 macrophages in phagocytosis; however, no significant cytotoxici

1 macrophages in phagocytosis; however, no significant cytotoxicity in survival was observed in these cells

[12]. We then studied the potential effect of surface modification on QD-mediated cytotoxicity to macrophages. A small number of J774A.1 cells in 6-well plates (5.0 × 104/well) were seeded and treated with QD particles precoated with PEG, PEG-NH2, or PEG-COOH, and the cells were then observed for 5 days. As shown in Figure 1A, the number of cells upon QD-PEG or QD-PEG-COOH treatment was 21.4 × 104 and 19.3 × 104, similar to that in the control (P > 0.05); however, the number of cells treated with QD-PEG-NH2 was 4.7 × 104, much lower than that in the control (P < 0.001). Moreover, the relative cellular flat surface area was measured with the Image-Pro-Plus software (Media Emricasan in vitro Cybernetics, Rockville, MD, USA), and the results indicated that the average size per cell was reduced by approximately 20% compared to the control (Figure 1A,B, P < 0.05). To tease apart the mechanisms responsible for the cytotoxicity of QD-PEG-NH2 to J774A.1 macrophages, we individually assessed cell proliferation and apoptosis. The BrdU incorporation check details assay indicated that the cell division of J774A.1 cells upon QD-PEG-NH2 exposure for 24 h was greatly diminished by approximately

40% compared to the control (P < 0.001), and cell growth was rarely affected in cells treated with QD-PEG or QD-PEG-COOH (Figure 1C), suggesting a robust inhibition of QD-PEG-NH2 on cell proliferation. To exclude

possible involvement of cell death induced by QD-PEG-NH2, we therefore surveyed Doramapimod nmr apoptosis and necrosis with FACS analysis after PI and FITC-conjugated Annexin V staining. Annexin V binds to phosphatidylserine that localizes on the outer surface of cell membrane, which is an early event in apoptosis and PI stains nucleus of necrotic cells [23]. As shown in Figure 2, the proportion of cells representing early apoptosis (Q4 region, Annexin V+PI−), necrosis (Q1 region, Annexin V-PI+), and late apoptosis or necrosis (Q2 region, Annexin V+PI+) remained similar among different treatments after 24 h compared Rebamipide to the control, demonstrating that QDs with these kinds of surface modifications exerted no cell death to J774A.1 cells. Figure 1 Biological influence of QDs on J774A.1 cells. (A) Bright field images of J774A.1 cells treated with QDs with different surface modifications at 47 μg/ml for 5 days (×40). (B) The bar graph represents the relative cellular flat surface area of J774A.1 cells treated with 47 μg/ml QDs coated with PEG-NH2 for 5 days (n = 50). (C) Cell proliferation was evaluated with the BrdU incorporation assay upon treatment with 47 μg/ml QDs with different surface modifications for 24 h (n = 6). Asterisk indicates P < 0.001. Figure 2 Cell death of J774A.1 cells in response to QD treatment. Representative images of cell death of J774A.

0; elution buffer) Fractions that mainly contained

0; elution buffer). Fractions that mainly contained rPnxIIIA were monitored

and confirmed by SDS-PAGE. For purification of rPnxIIIE, buy Crenolanib E. coli BL21-AI cultures harboring pET-Pnx3E were extracted in a binding buffer containing 6 M guanidine hydrochloride, and the extracts were purified with an elution buffer containing 6 M urea, similar to the method used to purify rPnxIIIA. The solvent of rPnxIIIA and rPnxIIIE was exchanged to a buffer containing 20 mM Tris-HCl and 150 mM NaCl by using FPLC and dialysis, respectively. Purification of native rPnxIA and rPnxIIA was performed briefly according to previous described methods [13]. Generation of deletion mutants of rPnxIIIA variants To compare the function of the unique selleck products repeat sequences

in the rPnxIIIA variants, deletion mutant rPnxIIIA expression vectors were constructed. In brief, deletion mutant expression vectors pBAD-Pnx3A209, which lacked amino acid residues of a repeat sequence at position 287-735 (Figure 1B; Repeat 1), and pBAD-Pnx3A197, which lacked amino acid residues of a repeat sequence at position 1097-1666, (Figure 1B; Repeats 2 and 3) were directly constructed using the wild-type protein expression vector pBAD-Pnx3A as the template with primer pairs pnx3A-209-f and pnx3A-209-r and pnx3A-197-f and pnx3A-197-r, respectively. A PrimeSTAR Mutagenesis Basal Kit (Takara Bio) was used to create these deletion mutant expression vectors. Finally, BAY 73-4506 in vitro pBAD-Pnx3A151, which lacked both repeat sequences, was constructed with the primer pair pnx3A-197-f and pnx3A-197-r with pBAD-Pnx3A209 as the PCR template. All the constructs were confirmed with DNA sequencing. The expression and purification of rPnxIIIA variants were performed in the same manner as that used for the wild-type rPnxIIIA. Cytotoxicity assay The cytotoxicity of the recombinant Pnx proteins toward J774A.1 cells was determined via a LDH

release assay that was performed according to the methods of Basler et al. [34] with minor modifications. Prior to incubation, the concentration of J774A.1 cells in a 96-well plate was adjusted 1 × FAD 105 cells per well. The cells were grown in fresh DMEM supplemented with 20 mM CaCl2 and appropriate antibiotics. rPnxIIIA was added to the wells such that its concentrations were 0.1, 0.5, and 1.0 μg/ml of the final concentrations. The plate was incubated at 37°C in 5% CO2 for up to 24 h. LDH release from the J774A.1 cells was measured at 1, 2, 4, 6, 12, and 24 h by using the supernatant from the treated cells; a cytotoxicity detection kit (Roche Diagnostics, Mannheim, Germany) was used for this purpose. For the comparison of cytotoxicity among rPnxIA, rPnxIIA, and rPnxIIIA, 1.0 μg/ml of each recombinant protein was incubated with the J774A.1 cells for 4 h. Thereafter, LDH release from the J774A.1 cells was measured. Furthermore, to assess the effect of existence of CD11a on inhibition of rPnxIIIA-induced cytolysis, LDH release from the J774A.

The elastic moduli and viscosity of TMV superlattice were determi

The elastic moduli and viscosity of TMV superlattice were determined to be E 1s   = 2.14 GPa, E 2s  = 21.3 MPa, and η s   = 12.4 GPa∙ms. From the characterized viscoelastic parameters, it can be concluded that the TMV/Ba2+ superlattice was quite rigid at the initial contact and then experienced a large deformation under a constant pressure. Finally, the simulation of the mechanical behavior of TMV/Ba2+ superlattice

under various loading cases, including uniform tension/compression and nanoindentation, were conducted to predict the mechanical response of sample under different loadings. The storage and loss shear moduli were also demonstrated to extend the applicability of the proposed method. With the selleck screening library characterized viscoelastic properties of TMV superlattice, we are now able to predict the process of tissue regeneration around the superlattice where the time-dependent mechanical properties of scaffold interact with the growth of tissue. Appendix Modeling of adhesive contact of viscoelastic

bodies The functional equation method was employed to develop a contact mechanics model for indenting a viscoelastic material with adhesion. A modified standard solid model was used to extract the viscous and elastic parameters of the sample. Several adhesive contact models are available, such as Johnson-Kendall-Roberts (JKR) model [50], Derjaguin-Muller-Toporov (DMT) model [46], etc. [51–53]. Detailed comparisons can be selleck chemicals found in reference [54]. As the DMT model results in a simpler differential equation, it was used in this study for the simulation to solve the indentation on an elastic body with adhesion. For the DMT model [46], the selleck inhibitor relation between the indentation force F and relative approach (-)-p-Bromotetramisole Oxalate δ, shown in Figure 8, can be expressed as Figure 8 Schematic of contact between a rigid sphere and a flat surface (cross-section view). (A.1) where R is the nominal radius of the two contact

spheres of R 1 and R 2, given by R = R 1 R 2/(R 1 + R 2); the adhesive energy density w is obtained from the pull-off force F c , where F c  = 3πwR/2; and the reduced elastic modulus E * is obtained from the elastic modulus E s and Poisson’s ratio ν s of the sample by with the assumption that the elastic modulus of the tip is much larger than that of the sample. In Equation (A.1), E * , which governs the contact deformation behavior, is decided by the sample’s mechanical properties. In the functional equation method [43], E * needs to be replaced by its equivalence in the viscoelastic system, so that the contact deformation behavior can be governed by the viscoelastic properties. To achieve it, the elastic/viscoelastic constitutive equations are needed. As a premise of the functional equation method, quasi-static condition is assumed so that the inertial forces of deformation can be neglected [43, 44]. The general constitutive equations for a linear viscoelastic/elastic system in Cartesian coordinate configuration can be written as (A.2) (A.

Thus, vitamin D insufficiency or deficiency may not have been a m

Thus, vitamin D insufficiency or deficiency may not have been a major factor for the lack of effects of isoflavones. (3) We did not collect data on hot flashes that could have served as a reflection of the biological effect and the appropriateness of the dosage of the isoflavones used in this study, in addition to this website the serum levels of isoflavones. (4) We used three different models of instruments from three different manufacturers to measure BMD. The variations among the three instruments may have masked the effects of soy isoflavones. However, we performed BMD measurements according to the International Society of Clinical

Densitometry guidelines. The instruments had daily quality checks and were operated by the same technologists throughout the period of study. The results within each center were analyzed separately and did not show any trend of effects. (5) A lack of total proximal femur BMD data from one center may have reduced the power to estimate the effect of soy isoflavones. However, it is difficult to perceive how isoflavone treatment

could improve proximal femur BMD while providing no C646 benefit in preventing bone loss at the lumbar spine. (6) Our sample size was not sufficient to analyze the effects of soy isoflavone on buy URMC-099 fracture rates. The fracture incidence in our study appeared higher than the results reported by a prospective study in Shanghai, China [41]. It should be noted that our study included only osteopenic or osteoporotic women, whereas the study in Shanghai included a cohort from the general population. However, in view of 64% increase in bone fracture rate in the isoflavone arm compared with that of the

placebo arm, more cautious monitoring in this regard is warranted in the future studies. Conclusions The current double-blind, randomized, placebo-controlled study of soy-extracted isoflavones on bone health failed to detect either an antiresorptive or a bone-sparing effect, despite possessing the strengths of larger dose, long observation period, and high compliance rate. Acknowledgments Thymidine kinase We would like to thank the three local hospitals, National Taiwan University Hospital, Changhua Christian Hospital, and Cheng Kung University Hospital, for their support in clinical observation and laboratory tests; we also appreciate the assistance of Taiwan Biotech Co. Ltd, Taiwan for its generous provision of isoflavones. Additionally, the authors are grateful for all the subjects who participated in this study. Grand support This study was supported by GE-PP02 grant “A Taiwan Isoflavone Multicenter Study (TIMS)” from the National Health Research Institutes, Zhunan, Taiwan. The funding source supervised the design, conduct, management and analysis, but was not involved in the interpretation of the study result. Conflicts of interest None.