This is important because some

This is important because some STAT inhibitor of the risk factors affect the risk of death as well as the fracture risk. Examples include increasing age, sex, low BMI, low BMD, use of glucocorticoids and smoking. Fig. 10 The risk of hip fracture with age in a model that considers 10-year fracture risk alone (the Garvan tool) and FRAX which computes the probability of hip fracture from the fracture and death hazards (FRAX). The T-scores are set differently in the two models so that the risks

are approximately equal at the age of 60 years. Data are computed from the respective websites [127]. With kind permission from Springer Science and Business Media General management Mobility and falls Immobilisation is an important cause of bone loss. Immobilised patients may lose as much bone in a week when confined to bed than they would otherwise lose in a year. For this reason, immobility

should, wherever possible, be avoided. The amount of weight-bearing exercise that is optimal for skeletal health in patients with osteoporosis is not known, but exercise forms an integral component of management [128–130]. Physiotherapy is an important component of rehabilitation after fracture. At all times, increased strength may prevent falls by improving confidence and coordination as well as maintaining bone mass by stimulating bone formation and by decreasing bone resorption, Citarinostat datasheet and by preserving muscle strength. Such measures together can be coupled with a programme to reduce the likelihood of falls in those at high risk. Risk factors for falling are shown in Table 10 [131]. Modifiable factors such as correcting decreased visual acuity, reducing consumption of medication that alters alertness and balance and improving the home environment (slippery floors, obstacles, insufficient lighting, handrails) are important measures aimed at preventing falls [132, 133]. Although large trials have shown that it is possible Montelukast Sodium to reduce falls [134, 135], randomised studies have not shown any significant decrease in fracture risk. Some randomised trials have shown that wearing hip protectors can markedly reduce hip fracture risk, particularly in the elderly

living in nursing homes. A meta-analysis of well-conducted randomised controlled trials has, however, cast some doubt about the anti-fracture efficacy of this preventive measure [136–139]. Table 10 Risk factors associated with falls (adapted from [131] with permission from Elsevier) 1. Impaired mobility, disability 2. Impaired gait and balance 3. Neuromuscular or musculoskeletal disorders 4. Age 5. Impaired vision 6. Neurological, heart disorders 7. History of falls 8. Medication 9. Cognitive impairment Nutrition At every stage of life, adequate dietary intakes of key bone nutrients such as calcium, vitamin D and protein contribute to bone health and reduce thereby the risk of osteoporosis and of fracture later in life [140].

If free Fe2+

is present in the cell, the produced H2O2 ca

If free Fe2+

is present in the cell, the produced H2O2 can form hydroxyl radicals (·OH), which may directly damage DNA. This may explain the induced production of Dps that reversibly binds iron. The produced H2O2 can be selleck removed by catalase (KatA) which converts H2O2 to H2O and O2[37, 57]. In contrast to a transcriptional study where an up-regulation of katA gene was noticed after acid exposure [24], induction of KatA was not observed in this proteomic study. Since C. jejuni is sensitive towards oxygen and lacks numerous oxidative stress regulators such as SoxRS and OxyR [13], the cell might be in a constantly oxygen-alert state in order to remove reactive oxygen species and damaging components from acid stress. No induction of heat RSL3 clinical trial shock proteins (Hsps) as chaperones or proteases were observed during acid stress in this study. A transcriptional study found an up-regulation of clpB, dnaK, grpE, groEL/ES and htrA[24]. One explanation could be the sensitivity of 2D-gel-electrophoresis for proteomic analysis as mentioned Barasertib price above and the detection limit due to molecular size and isoelectric point (pI) of the proteins. The Hsps, ClpP and GroES have molecular masses

close to the maximum and minimum detection size, respectively, and HtrA has a pI of 9.6 which is outside the pI range of the system used here. Acid exposure of C. jejuni NCTC 11168 was related to changes in gene expression and synthesis of acid stress proteins. However, comparison of the proteomic and transcription study showed a limited correlation between induced proteins and over-expression of genes. A recent proteomic study with acid adaptation of Salmonella enterica also [26] found a limited correlation between the outcomes of the transcriptional (qRT-PCR) versus translational (2D-gel) studies. The lack of corresponding

results may be due to the lifetime of the RNA and crotamiton the time from transcription to translation. Conclusions It can be concluded that the three C. jejuni strains, at the phenotypic and proteomic level, responded differently to the acid stresses. We demonstrated that acid stress induces production of several proteins normally involved in iron control and oxidative stress defence in C. jejuni. This work has contributed to the understanding of what occurs in the C. jejuni cells during acid stress. Acknowledgements This work was financially supported by the Danish Food Industry Agency. We acknowledge Bjarne Albrektsen for excellent technical assistance during development and optimization of the chemically defined broth; Andrea Maria Lorentzen from the University of Southern Denmark, who has been a great help in identifying proteins; and Søs Inger Nielsen for excellent technical assistance with qRT-PCR runs. Dr. Thomas Alter, Freie Universitet Berlin, generously provided the strains 305 and 327. References 1. Birk T, Knøchel S: Fate of food-associated bacteria in pork as affected by marinade, temperature, and ultrasound.

This study is a contribution to the ANR AQUAPHAGE

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Statistical significance was declared at P < 0 05 Results Time t

Time to exhaustion was not normally distributed and was therefore analysed using the Wilcoxon signed rank test. Statistical significance was declared at P < 0.05. Results Time to Fatigue and ratings 4EGI-1 order of perceived exertion Time to fatigue

during constant-load exercise was similar between the two fat trials [(Control trial: 116(88-145) min; F trial: 122(96-144) min; FC trial: 127(107-176) min)]. Ratings of perceived leg exertion were significantly lower (F(1,9) = 11.985, P = 0.007) during constant-load exercise on the FC compared with the F trial while ratings of perceived breathlessness were not different between the trials (Figure 1). Six out of ten subjects ranked the FC as the easiest trial (one subject was unsure). Figure 1 Ratings of perceived exertion, for leg muscular discomfort SRT2104 solubility dmso (top panel) and breathlessness (bottom panel). *: indicates a significant difference between the F (white dots) and the FC (black dots) trials. §: indicates significant differences within the trials compared with the 15 min time-point. The dash line indicates the Control trial. Values are AZD8931 solubility dmso presented as the mean ± SD. Cardiopulmonary

variables and fuel oxidation O2 increased over time on both trials and it was higher on the FC trial compared with the F trial (F(1,9) = 7.980, P = 0.02) (Table 1). Minute ventilation ( E) was significantly higher on the FC trial compared with F trial (F(1,9) = 10.917, P = 0.009) and there was a progressive increase in E and co2 over time on both fat trials; no differences in respiratory exchange ratio (RER) were found between F and FC trials (Table 1).     Exercise Time (min) Variables Trials Rest 15 30 45 60 75 90 O2 (L·min-1) Control .3 ± .04 3.2 ± 0.4 3.2 ± 0.4 3.4 ± 0.5 3.4 ± 0.5 3.5 ± 0.6 3.4 ± 0.4   F .3 ± .03 3.1 ± 0.4 3.2 ± 0.4§ 3.2 ± 0.4 3.4 ± 0.4§ 3.4 ± 0.5§ 3.5 PI-1840 ± 0.5§   FC .4 ± .07 3.3 ± 0.3 3.4 ± 0.4 3.4 ± 0.5§ 3.5 ± 0.5§ 3.6 ± 0.5*§ 3.6 ± 0.5§ CO2 (L·min-1) Control .3 ± .04 3.0 ± 0.5 3.0 ± 0.5 3.1 ± 0.5 3.1 ± 0.5 3.2 ± 0.7 3.1 ± 0.5   F .3 ± .03 3.0 ± 0.4 3.1 ± 0.4 3.1 ± 0.4 3.2 ± 0.4§ 3.2 ± 0.4§ 3.3 ± 0.5§   FC .3 ± .05 3.0 ± 0.3 3.1 ± 0.4 3.1 ± 0.4 3.2 ± 0.4 3.3 ± 0.5§ 3.2 ± 0.4 E (L·min-1) Control 8.0 ± 2 66 ± 1 69 ± 1 73 ± 1 74 ± 1 78 ± 1 76 ± 9.0   F 8.0 ± 1 66 ± 1 68 ± 1 70 ± 1§ 73 ± 1§ 76 ± 1§ 78 ± 14§   FC 10 ± 2 70 ± 6 73 ± 8*§ 75 ± 1*§ 79 ± 1*§ 81 ± 1*§ 81 ± 10§ RER Control .89 ± .08 .95 ± .3 .95 ± .03 .94 ± .05 .94 ± .03 .93 ± .04 .93 ± .02   F .87 ± .10 .95 ± .3 .94 ± .03 .93 ± .04 .93 ± .03§ .93 ± .02 .91 ± .03§   FC .87 ± .07 .93 ± .4 .91 ± .03§ .91 ± .05 .91 ± .05 .90 ± .06 .88 ± .05§ Values are presented as the mean ± SD *: Indicates a significant difference from the F trial at the same time-point.

Payne JW, Smith MW: Peptide transport by microorganisms Adv Micr

Payne JW, Smith MW: Peptide transport by microorganisms. Adv Microb Physiol 1994, 36:1–80.PubMedCrossRef 22. Linton KJ, Higgins CF: The Escherichia coli ATP-binding cassette

(ABC) proteins. Mol Microbiol 1998, 28:5–13.PubMedCrossRef 23. Martin SA: Nutrient transport by ruminal bacteria – a review. J Anim Sci 1994, 72:3019–3031.PubMed 24. Pressman BC: Ionophorous antibiotics as models for biological transport. Fed Proc 1968, 27:1283–1288.PubMed 25. Russell JB, Strobel HJ: Mini-review: The effect of ionophores on ruminal fermentation. Appl Environ Microbiol 1988, 55:1–6. 26. Horler DF, Poziotinib chemical structure Westlake DW, McConnel WB: Conversion of glutamic acid to volatile acids by micrococcus aerogenes. Can J Microbiol 1966, 12:47–53.PubMedCrossRef 27. Buckel W: Analysis of the fermentation pathways of clostridia using double labeled glutamate. Arch Microbiol 1980, 127:167–169.PubMedCrossRef 28. Prins

RA, Van Gestel JC, Counotte GHM: Degradation of amino acids and peptides by mixed rumen microorganisms. Z Tierphysiol Tierernahr Futtermittelkd 1979, 42:333–339.PubMedCrossRef 29. Wallace RJ: Ruminal microbial metabolism of peptides and amino acids. J Nutr 1996, 126:1326S-1334S.PubMed 30. Armstead IP, Ling JR: Variations in the uptake and metabolism of peptides and amino acids by mixed ruminal bacteria in vitro. Appl Environ Microbiol 1993, 59:3360–3366.PubMed 31. Ling JR, Armstead IP: The in vitro uptake and metabolism of peptides and amino acids by five species of rumen bacteria. J Appl Bacteriol 1995, 78:116–124.PubMedCrossRef 32. Bladen selleck kinase inhibitor HA, Bryant MD, Doetsch RN: A study of bacterial species from the rumen which produce ammonia from protein hydrolyzate. Appl Microbiol 1961, 9:175–180.PubMed 33. Chen M, Wolin MJ: Effect of monensin and lasalocid-sodium on the growth of methanogenic and rumen saccharolytic bacteria. Appl Environ

Microbiol 1979, 38:72–77.PubMed 34. McDevitt RM, Brooker JD, Acamovic T, Sparks NHC: Necrotic enteritis; a continuing challenge for the poultry Adriamycin datasheet industry. World’s Poultry Sci J 2006, 62:221–247.CrossRef 35. Macfarlane GT, Gibson GR: Bacterial infections and diarrhea. In Human colonic bacteria: role in nutrition, physiology, and pathology. Edited by: Gibson GR, Macfarlane GT. Boca Raton, Florida: CRC Press; 1995:201–226. 36. Chen GJ, Glycogen branching enzyme Russell JB: Transport and deamination of amino acids by a gram-positive, monensin-sensitive ruminal bacterium. Appl Environ Microbiol 1990, 56:2186–2192.PubMed 37. Chen G, Russell JB: Effect of monensin and a protonophore on protein degradation, peptide accumulation and deamination by mixed ruminal microorganisms in vitro. J Anim Sci 1991, 69:2196–2203.PubMed 38. Wallace RJ, Czerkawski JW, Breckenridge G: Effect of monensin on the fermentation of basal rations in the rumen simulation technique (rusitec). Br J Nutr 1981, 46:131–148.PubMedCrossRef 39. Whitehead R, Cooke GH, Chapman BT: Problems associated with the continuous monitoring of ammoniacal nitrogen in river water.

pylori culture, one each from the antrum, corpus, and cardia The

pylori culture, one each from the antrum, corpus, and cardia. These were stained with haematoxylin and eosin and reviewed for the H. pylori-related histology by the updated Sydney’s system [4, 22, 23]. In addition, the study collected 181 H. pylori isolates for the detection of dupA genotype by PCR. One hundred and three isolates were collected from randomly selected patients who had agreed

to undergo SNP analysis, while 78 isolates were from patients without SNP analysis. The H. pylori culture were conducted from the two additional gastric biopsies collected during the same endoscopy and processed with the method applied in previous publications [4, 22]. For those with positive H. pylori culture, the isolates were extracted for genomic DNA to be analyzed for the dupA genotypes by PCR. The extraction of DNA was done with the same method as described previously [4, 22]. Positive H. pylori infection was defined by positive histology or culture. Genotypes of SNPs in MMPs and TIMPs Peripheral blood 8 ml was obtained from each subject for genomic DNA, which was extracted from peripheral blood mononuclear cells according Selleck HDAC inhibitor to the manufacturer’s instructions (Viogene, Taipei, Taiwan). Five SNPs in

MMP-3-1612 5A/6A, MMP-7-181 A/G, MMP-9exon 6 A/G, Wnt tumor TIMP-1372 C/T, and TIMP-2-418 G/C polymorphisms were determined by PCR-RFLP assays [18, 24–26]. Using the extracted DNA as template, the regions of each MMP and TIMP were amplified by PCR using commercially available kits (GoTaq® Green Master Mix, Promega, Madison, WI, USA) following the manufacturer’s instructions. The sequences of primers, PCR conditions, and restriction enzymes (obtained from New England Biosciences, U.S.) used were summarized in Table 1. After digestion, the products were separated by electrophoresis on a 4% agarose gel. The MMP and TIMP genotypes were shown as different gel examples (Figure 1). Table 1 The PCR primers

used in the study SNP/gene Primer sequence (5′ →3′) Size (bp) Restriction enzyme Reference MMP-3 -1612 5A/6A GATTACAGACATGGGTCACG 120 Xmn I Shibata et al, 2005   TTTCAATCAGGACAAGACGAAGTTT   6A: 120 bp         5A: 97 bp + 23 bp   MMP-7 -181 A/G TGGTACCATAATGTCCTGAAT Phosphoglycerate kinase 150 EcoR I Jormsjö et al, 2001   TCGTTATTGGCAGGAAGCACACAATGAATT   A: 150 bp         G: 120 bp + 30 bp   MMP-9 exon6 A/G CCATCCATGGGTCAAAGAAC 295 Sma I Shibata et al, 2005 *   GGGCTGAACCTGGTAGACAG   A: 295 bp         G: 192 bp + 103 bp   TIMP-1 372 C/T GCACATCACTACCTGCAGTC 175 BssSI Wollmer et al, 2002   GAAACAAGCCCACGATTTAG   T: 175 bp         C: 152 bp + 23 bp   TIMP-2 -418 G/C CGTCTCTTGTTGGCTGGTCA 304 BsoBI Zhou et al, 2004   CCTTCAGCTCGACTCTGGAG   C: 253 bp + 51 bp         G: 230 bp + 51 bp + 23 bp   jhp0917_1 TGGTTTCTACTGACAGAGCGC 307 – Lu et al.

8 ± 0 3 11 5 ± 0 5 0 20 ± 0 07 0 40 ± 0 02 0 20 ± 0 02 0 57 ± 0 0

8 ± 0.3 11.5 ± 0.5 0.20 ± 0.07 0.40 ± 0.02 0.20 ± 0.02 0.57 ± 0.03 MF 27.31 ± 1.5 46.02 ± 2.3 0.60 ± 0.03 0.70 ± 0.07 0.13 ± 0.08 0.75 ± 0.04 Yx/s indicates g of dry biomass produced per g of substrate; Yp/s indicates g of lactic acid

produced per g of substrate. Values are an average of 3 different experiments. EPS production and purification The EPSs content in the fermentation Selleckchem PND-1186 broth ranged between 200–400 mg⋅l−1 and the initial protein titre was estimated up to 50 fold. Protease was used to eliminate these major contaminants of the exopolysaccarides, and the following tangential ultrafiltration (UF)/ diafiltration (DF) was performed to further purify the product and to remove salt and other smaller contaminants. During UF the flux decreased

from 8.3 to 7.3 l∙m−2 h−1 and it increased again to 13.5 l∙m−2 h−1 during the DF phase that lasted until reaching a conductivity of 0.8mS/cm. The supernatant was concentrated 9 fold compared to the initial volume. The recovery yield after membrane purification was on average 85% and the purified EPSs solution had a protein content that was inferior to 0.5% w/w. Structure determination of see more mannan polymer Compositional and methylation analyses showed the presence of different derivatives of mannose, such as terminal Manp, 2-substituted Manp, 3-substituted Manp, 6-substituted Manp and 2,6-substituted Manp. On this ground, it could be deemed the presence of a very intricate polymer only based on a mannose monosaccharide, in which other mannose branching residues were attached to a mannan backbone. The polysaccharide underwent Nuclear Magnetic MLN2238 in vivo Resonance (NMR) analysis and even though the 1H- (Figure 4) and 13C-NMR spectra appeared rather complex, it was clearly related

to the mannan polysaccharides already described [26]. 2D NMR and degradation procedures confirmed the structure, a 6-substituted mannan backbone very with small branching chains (one to three units) of Manp residues (Figure 4). Figure 4 Characterization of the EPS produced by L. crispatus L1. 1H-NMR spectrum and spin system attribution for each sugar of the mannan polysaccharide and structure of the EPS. Inhibition of C. albicans adhesion to Vk2/E6E7 C. albicans is a constituent of the vaginal microbiota and, as opportunistic pathogen, it causes genital infections in humans. In immuno-compromised individuals, overgrowth of the fungus results in candidiasis. C. albicans pathogenecity depends on several virulence traits that allow the fungus to invade new tissues, evade the immune system of the host, and facilitate the infection [27]. To verify the antagonist effect of L. crispatus L1 against C. albicans, the influence of the strain on the adhesion capacity of C. albicans to immortalized human vaginal epithelial cell line was evaluated. The results demonstrate that there is a significantly reduced adhesion of C.

Armamento-Villareal R, Napoli N, Diemer K, Watkins M, Civitelli R

Armamento-Villareal R, Napoli N, Diemer K, Watkins M, Civitelli R, Teitelbaum S, Novack D (2009) Bone turnover in bone biopsies of patients with low-energy cortical fractures receiving bisphosphonates:

a case series. Calcif Selleck mTOR inhibitor Tissue Int 85:37–44CrossRefPubMed 26. Goh SK, Yang KY, Koh JS, Wong MK, Chua SY, Chua DT, Howe TS (2007) find more subtrochanteric insufficiency fractures in patients on alendronate therapy: a caution. J Bone Joint Surg Br 89:349–353CrossRefPubMed 27. Ing-Lorenzini K, Desmeules J, Plachta O, Suva D, Dayer P, Peter R (2009) Low-energy femoral fractures associated with the long-term use of bisphosphonates: a case series from a Swiss university hospital. Drug Saf 32:775–785CrossRefPubMed 28. Kwek EB, Goh SK, Koh JS, Png MA, Howe TS (2008) An emerging pattern of subtrochanteric stress fractures: a long-term complication of alendronate therapy? Injury 39:224–231CrossRefPubMed 29. Lenart BA, Neviaser AS, Lyman S, Chang CC, Edobor-Osula buy STI571 F, Steele B, van der Meulen MC, Lorich DG, Lane JM (2009) Association of low-energy femoral fractures with prolonged bisphosphonate use: a case control study. Osteoporos Int 20:1353–1362CrossRefPubMed 30. Neviaser AS, Lane JM, Lenart BA, Edobor-Osula F, Lorich DG (2008) Low-energy femoral shaft fractures associated

with alendronate use. J Orthop Trauma 22:346–350CrossRefPubMed 31. Odvina CV, Zerwekh JE, Rao DS, Maalouf N, Gottschalk FA, Pak CY (2005) Severely suppressed bone turnover: a potential complication of alendronate therapy. J Clin Endocrinol Metab 90:1294–1301CrossRefPubMed 32. Fielding JW, Magliato HJ (1966) Subtrochanteric fractures. Surg Gynecol Obstet

122:555–560PubMed 33. Muller ME, Nazarian S, Koch P, Schatzker J (1990) The AO classification of long bones. http://​aofoundation.​com/​AOFileServer/​PortalFiles?​FilePath=​/​Extranet/​en/​_​att/​wor/​act/​fracture_​classif/​mueller_​ao_​class.​pdf. Accessed 23 Sep 2010 34. Seinsheimer F (1978) Subtrochanteric fractures of the femur. J Bone Joint Surg Am 60:300–306PubMed 35. Black DM, Genant HK, Bucci-Rechtweg C, Bauer DC, Mesenbrink PG, Palermo L, Nusgarten L, Eastell R (2009) Does zoledronic acid increase risk of atypical subtrochanteric femoral OSBPL9 shaft fractures? Results from the HORIZON-PFT. J Bone Miner Res 24 (Suppl 1). http://​www.​asbmr.​org/​Meetings/​AnnualMeeting/​AbstractDetail.​aspx?​aid=​918d35dd-6a3d-43f6-b35f-b484a15b81cf. Accessed 23 Sep 2010 36. Bunning RD, Rentfro RJ, Jelinek JS (2010) Low-energy femoral fractures associated with long-term bisphosphonate use in a rehabilitation setting: a case series. PM&R 2:76–80CrossRef 37. Capeci CM, Tejwani NC (2009) Bilateral low-energy simultaneous or sequential femoral fractures in patients on long-term alendronate therapy. J Bone Joint Surg Am 91:2556–2561CrossRefPubMed 38. Koh JS, Goh SK, Png MA, Kwek EB, Howe TS (2010) Femoral cortical stress lesions in long-term bisphosphonate therapy: a herald of impending fracture? J Orthop Trauma 24:75–81CrossRefPubMed 39.

plantarum MYL26 to see which cellular parts contributed mostly to

plantarum MYL26 to see which cellular parts contributed mostly to LPS tolerance induction. In contrast with our expectations, although intracellular extract and genomic DNA induced IκBα expression more significantly than that of control group, they failed to activate TOLLIP, SOCS1, and SOCS3. There are five TLRs (TLR2/ 4/ 5/ 7/ 9) sharing similar

downstream signal pathway (MyD88, IRAK, TRAF, IKK, NFκb) [38]. Except for IκBα which directly binds to NFκb, the negative regulators TOLLIP, SOCS1, and SOCS3 are well-established having abilities in interference with recruitment of MyD88 and IRAK. It has been reported that TOLLIP, SOCS1, and SOCS3 not only attenuate TLR4 signaling, Selleckchem AZD4547 but also have impact on TLR2/5/7/9

signaling [39, 40]. Briefly, L. plantarum MYL26 intracellular extract and genomic DNA activate TLRs-NFκb pathways other than TLR4 (TLRs cross-tolerance), but they did not attenuate inflammation through induction of TOLLIP, SOCS1, and SOCS3. Taken together, we proposed that L. plantarum MYL26 intracellular extract and genomic DNA induced LPS tolerance through pathways different from induction of Tollip, SOCS-1 and SOCS-3, which were key negative regulators activated by live/dead L. plantarum MYL26 and cell wall components. One of the limitations of this study is that the causes of IBD, other than breakdown of LPS tolerance, are multifaceted. Several lines of evidence has pointed out that Urocanase in addition to inherited factors, pollution, drugs, diets, breastfeeding, even emotional stress, could be responsible for genetically failing to interpret molecular microbial patterns appropriately, thus leading to

irregular innate and adaptive immune responses [41, 42]. The second limitation is that PAMPs other than LPS induce GI inflammation through different pathways. Criteria for probiotic selection of LPS tolerance induction strains might be not suitable with respect to inflammation symptoms caused by other PAMPs. Conclusions The administration of lactic acid bacteria in patients suffering from GI disorders regularly depends on try-error methods, and numerous probiotics treatment applied to clinical trials showed frustrated results, which perhaps might be related to the fact that the probiotic screening criteria is generally based on susceptibility to artificial GI environments (acid and bile resistance) or adhesive properties instead of on immunomodulatory capacities, for instance, induction of LPS tolerance. Our research provided a new insight to describe the L.

Nano Letters 2010, 10:2323–2329 CrossRef 22 Peng KQ, Huang ZP, Z

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