In summary, the mutations either had no influence on the survival under pH stress conditions or improved resistance towards pH stress. Figure 4 Resistance towards pH stress. The bacteria were grown in Middlebrook 7H9 broth with OADC at pH 7 and pH 5 during 11 days; the ATP content was recorded by quantification of the amount of ATP in the cultures. The amount of ATP is represented

as RLU (relative light units). A: WT and mutant MAV_1778; B: WT and mutant MAV_3128; C: WT and mutant MAV_3625; D: WT and mutant MAV_2599. Amoeba plating test Free-living amoebae are known to host environmental mycobacteria including M. avium, which are able to survive in Acanthamoeba trophozoites as well as in the exocysts [4,

60, 61]. Growth in Acanthamoeba was associated with subsequently enhanced Selleck Palbociclib virulence in infection experiments with mice [62]. Since some virulence mechanisms are employed www.selleckchem.com/products/Etopophos.html by amoeba-resistant bacteria to survive in amoebae as well as in macrophages [4, 63–65], amoebae have been used as test systems for determination of bacterial virulence factors [40, 63, 66]. An Acanthamoeba castellanii agar plate assay was developed and successfully employed for screening of mutants of Legionella pneumophila[40]. We adapted this APT to fit the growth conditions (medium, temperature, duration) of M. avium and tested the eight mutants in comparison to the WT. After incubation for five to seven days at Doxacurium chloride 28°C, the WT formed colonies even if the cultures were diluted 1:103 before being dropped on the lawn of amoebae. The growth of some mutants was more strongly affected by the amoebae but a differentiated evaluation of the impact of the various mutations on survival in the amoebae

was not possible (data not shown). The APT thus was not sensitive enough to reveal differences in the capacity of the mutants to survive within the amoebae. This was surprising, because the APT has proven to be an efficient tool for the identification of virulence genes in L. pneumophilae[40]. There are several possible explanations for this discrepancy. Amoebae are the most important habitat of Legionella, while M. avium is not dependent on the presence of amoebae for survival and distribution. As a consequence, Legionella might have evolved more important virulence factors interacting with amoebae. Another possible explanation may result from the differences in the generation times of L. pneumophilae and M. avium. L. pneumophilae is a fast-growing bacterium forming clearly visible colonies few days after plating, while the slow-growing M. avium 104 requires two weeks to generate colonies of comparable size. This time span may be too long to maintain the amoebae as trophozoites actively interacting with the mycobacteria. In conclusion, we estimate the APT to be of only little value for the detection of virulence genes of slow-growing mycobacteria.

The mean pharmacokinetic values related to the terminal slope (AUCinf and t ½β) were therefore excluded because some participants demonstrated %AUCextrapolation >20 % (% of extrapolation part of AUCinf); in particular, only two subjects could be included for calculating half-life in the gemigliptin + glimepiride treatment group, and most subjects were excluded by this extrapolation (Table 2). Moreover, from this study, there might be a difference in the half-life of gemigliptin between treatment groups because almost all subjects were excluded from the analysis of the half-life

in the combination group compared with the monotherapy group. However, pharmacokinetic comparisons between treatment groups were based on AUC τ,ss (gemigliptin) or AUClast (glimepiride) and C max by protocol, and which values were calculated only see more observed data, not extrapolated. Therefore, further evaluation would be needed to obtain accurate pharmacokinetic parameters of gemigliptin related to the AUCinf and apparent terminal selleck compound half-life. The MRs of LC15-0636 to gemigliptin are also similar to previously reported MR values

(0.27 ± 0.10; Gemigliptin IB version 6.0, September 2012). As expected, glimepiride did not seem to affect the production of gemigliptin metabolites. Similarly, the MRs of M1 were the same (0.18 ± 0.03), regardless of the coadministration of gemigliptin. A previous study indicated that M1 is mainly formed by CYP2C9, and there are a number of reported genetic variants

of CYP2C9. Among these, the CYP2C9*2 and 3 alleles are known to markedly reduce the metabolism of glimepiride [35, 36]. The CYP2C9 polymorphism also demonstrates inter-ethnic differences. Among Caucasians, Sirolimus ic50 CYP2C9*2 demonstrates an allele frequency of 10–19 %, but is rare among East Asians [37]. The CYP2C9*3 heterozygous allele is only found in East Asians at a frequency of 1–6 % [38, 39]. This might be part of the reason for the differences in the pharmacokinetic values of glimepiride between previous studies and our own. Malerczyk et al. reported the pharmacokinetic parameters for glimepiride following the single-dose administration of 4 mg to healthy volunteers: mean C max of 307.8 μg/L and mean AUC of 1,297 μg/L · h for glimepiride, which were slightly higher than the results of our present study. Another study reported a geometric C max mean of 1,084 ng/mL and AUClast of 8,753 ng · h/mL, and the subjects were all Caucasian [20, 40]. Because the participants in this study were all Korean, most were expected to express the CYP2C9*1 allele, but we did not evaluate genotypes. Hence, differences between genotypes should be further evaluated. However, this is a crossover study, and the finding that glimepiride did not change due to gemigliptin administration is still valid even without genotype testing. Up to 8 mg/day of glimepiride can be administered, but the usual maintenance dose is 1–4 mg once daily.

Alternatively, the differences could reflect sample to sample variation. Partial canonical correspondence analysis (pCCA) of T-RFLP profiles As described above, endophytic bacterial communities varied with the time of sampling and the locations of host plants. To determine the relative importance of each factor, the relative abundances of each T-RF were used to conduct pCCA of T-RFLP profiles. Figure 2 (a) shows the pCCA of T-RFLP profiles of A. viridis treating sampling dates as the environmental factor with sampling locations as covariable. Because the

PD-1/PD-L1 signaling pathway first pCCA axis is more important than the second axis, the differences between samples from May and the other two months are more significant than the differences between samples from June and July, a result which is consistent with the summary statistics of T-RFs (Table 1). This result implies rapid early changes in the development of endophytic bacterial communities, consistent Sunitinib research buy with rapid plant growth of the host species, A. viridis. Permutation tests revealed sampling date is a significant factor (p-value = 0.0001). Figure 2 Partial Canonical Correspondence Analyses (pCCA) of T-RFLP profiles treating each of the three factors considered as the environmental factor. (a) pCCA of T-RFLP profiles

of A. viridis samples treating sampling date as the environmental factor. (b) pCCA of T-RFLP profiles of A. viridis treating sampling location as the environmental factor. (c) pCCA of T-RFLP profiles of all five host species samples treating host plant species as the environmental factor. The pCCA indicated that the three factors tested were all significant. pCCA Axes1 and 2 represent the two most important canonical correlations that explain the sample variation with pCCA Axis1 being the most important. The pCCA result of T-RFLP profiles of A. viridis treating location of host plants as environmental factor with sampling dates as covariable (Figure 2 (b)) indicated that the differences between samples from site 1 and other sites

were stronger than the differences between sites 2 and 3. Permutation tests revealed location of host plants was a significant factor (p-value = 0.0005). Extension of the analysis Niclosamide to multiple host species Having established month to month variation and sites as significant factors shaping endophytic bacterial communities in A. viridis, we asked whether the A. viridis communities were shared in other species growing at the same times in the same locations and whether those species had similar time and location influences on their community compositions. Host plant species may influence leaf endophytic bacterial communities because of their different physiological and biochemical features. Indeed, the T-RFLP patterns of A. viridis, A. psilostachya, and P. virgatum individuals were distinct (Figure 1(c)). The total number of T-RFs detected varied from 16 for R. humilis to 72 for A.

Insect Mol Biol 1992,1(1):49–52.CrossRefPubMed 24. Cheng L, Bartholomay L, Olson KE, Lowenberger C, Vizioli J, Higgs S, Beaty BJ, Christensen BM: Characterization of an endogenous gene expressed in Aedes aegypti using an orally infectious NVP-BGJ398 chemical structure recombinant Sindbis virus. J Insect Sci 2001.,1(10): Online. 25. Pierro DJ, Powers EL, Olson KE: Genetic determinants of Sindbis virus strain TR339 affecting midgut infection in the mosquito Aedes aegypti. J Gen Virol 2007,88(5):1545–1554.CrossRefPubMed 26. Xi Z, Ramirez JL, Dimopoulos G: The Aedes aegypti Toll pathway controls dengue virus infection. PLoS Pathog 2008,4(7):e1000098.CrossRefPubMed 27. Tschuch

C, Schulz A, Pscherer A, Werft W, Benner A, Hotz-Wagenblatt A, Barrionuevo L, Lichter P, Mertens D: Off-target effects of siRNA specific for GFP. BMC Mol Biol 2008,9(1):60.CrossRefPubMed 28. Robalino J, Bartlett T, Shepard E, Prior S, Jaramillo G, Scura E, Chapman RW, Gross PS, Browdy CL, Warr GW: Double-stranded RNA induces sequence-specific antiviral silencing in addition to nonspecific immunity in a marine shrimp: convergence of RNA interference and innate immunity in the invertebrate antiviral response? J Virol 2005,79(21):13561–13571.CrossRefPubMed check details 29. Pitaluga AN, Mason PW, Traub-Cseko YM: Non-specific antiviral response detected in RNA-treated cultured cells of the sandfly, Lutzomyia longipalpis. Dev Comp Immunol 2008,32(3):191–197.CrossRefPubMed 30. Franz A, Sanchez-Vargas

I, Adelman Z, Blair C, Beaty B, James A, Olson K: Engineering RNA interference-based

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Black bars = control, dark gray

bars = kanamycin (100 ug/ml), light gray bars = ampicillin (100 ug/ml) challenge. Number at the base of each bar denotes the number of independent replicates. cfu = colony forming unit. The results reinforce the concept that biofilm cultures can behave very differently from planktonic cultures and trends from planktonic cultures may not be relevant to biofilm cultures. Considering the well established importance of biofilms in medical infections, it is essential to test antimicrobial strategies against relevant microbe growth conditions. 2. Nutritional perturbations Surfaces susceptible to microbial colonization are often subjected to changing RXDX-106 mouse nutrient levels. For instance, a central venous catheter would experience different blood glucose levels based on patient activity, diel feeding schedules, or medical conditions like diabetes. Industrial food preparation surfaces could experience different nutrient loads based on worker schedules. The effect of nutritional environment perturbations on biofilm antibiotic tolerance

was assayed to determine if antibiotic efficacy would be predictable. Perturbing the nutritional environment by adding 10 g/L glucose to LB medium produced a large change in colony biofilm kanamycin and ampicillin tolerance (Fig. 2). In the presence of glucose, kanamycin reduced cfu’s per biofilm by approximately one order Saracatinib cell line of magnitude. This is in stark contrast with the 9 log10 decrease observed Meloxicam in the absence of glucose. In the presence of glucose, ampicillin produced a 7 log10 decrease in cfu’s per biofilm. For comparison, ampicillin produced a one order of magnitude reduction in cfu’s per biofilm when grown on LB only. Just prior to antibiotic challenge, the biofilm cultures grown on LB + glucose contained 8.9 ± 0.1 log10 cfu’s/biofilm while the LB only cultures contained

9.3 ± 0.1 cfu’s/biofilm. Changes in antibiotic tolerance were not likely due to different cell densities as reported with planktonic S. aureus cultures [19]. Interestingly, perturbing planktonic cultures with 10 g/L glucose had no statistically significant effect on kanamycin and ampicillin tolerance (Additional file 1, Fig. S1). The planktonic culture densities just prior to antibiotic challenge were 7.5 ± 0.4 log10 and 7.8 ± 0.2 log10 cfu/ml for the LB + glucose and LB only cultures respectively. Figure 2 Effect of glucose perturbation on wild-type E. coli K-12 biofilm antibiotic tolerance. Cultures were grown as biofilms for 6 hours before being transferred to antibiotic treatment plates for 24 hours. Conditions included only LB medium and LB medium supplemented with 10 g/L of glucose. Reported cfu/biofilm data was determined after treatment. Black bars = control, dark gray bars = kanamycin (100 ug/ml), light gray bars = ampicillin (100 ug/ml) challenge. Number at the base of each bar denotes the number of independent replicates. cfu = colony forming unit.

A significantly higher increase of ROS levels over time was observed in gup1∆ mutant in comparison AZD6738 chemical structure to Wt cells. The biggest difference was on day 6 (stationary phase), when the percentage of gup1∆ mutant cells exhibiting ROS accumulation was the twice (~80%) that of Wt cells (~40%). The mutant reached 100% of cells with ROS accumulation on day 10, while Wt took 17 days to reach that state (Figure 5A). Still regarding gup1∆ mutant, the 100% ROS was maintained till the end of experiment (more five days), which is in agreement

with the observed death of these strain cells (Figure 1 – after 12 days more than 99% death). The difference between Wt and gup1∆ mutant strains was also extremely notorious in acetic acid treated cells (Figure 5B). Soon after acetic acid addition, gup1∆ mutant exhibited ROS accumulation in ~ 8% of the cells, whereas Wt presented less than 1%. This difference was accentuated with time. At one hour treatment gup1∆ mutant cells with ROS accumulation

was higher than 30% and Wt cells less than 5%. Two hours treatment led to a substantial rise of ROS positive gup1∆ mutant cells (~85%) compared with only ~10% of Wt. At the end of the treatment, almost all gup1∆ mutant cells exhibited ROS accumulation, in clear contrast with the ~15% of ROS accumulation displayed by Wt strain (Figure 5B). Figure 5  GUP1  deletion promotes substantial ROS accumulation. Cells from chronological lifespan assay (A) and from acetic acid treatment (B) were analyzed for accumulation of ROS using DHE staining selleckchem by flow cytometry. At least 35,000 cells were analyzed. Data represent mean ± SD of at least 3 independent experiments. Discussion The finding of an endogenous PCD process with an apoptotic phenotype has turned yeast into a powerful model for apoptosis research

[39, 51, 52]. In fact, S. cerevisiae commits to cell death showing typical features of mammalian apoptosis, in response to different stimuli. However, how cell compounds participate in the processes leading to cell death in yeast remains to be established. Gup1p, an O-acyltransferase, is Rucaparib ic50 required for several cellular processes that are related to apoptosis development, namely, rafts integrity and stability, lipid metabolism including GPI anchor correct remodeling, proper mitochondrial and vacuole function, and actin dynamics [30, 31, 33, 35, 37, 42, 53–56]. In this work we used two known apoptosis-inducing conditions, chronological aging [6] and acetic acid [4], to assess several apoptotic markers in gup1∆ mutant strain. We found that, when compared with Wt, gup1∆ mutant presents a significant reduced chronological lifespan, showing almost no viability after 11 days incubation. Chronologically aged yeast cultures were shown to die exhibiting typical apoptotic markers [6].

52 Paragraph 2). Ministry of Health, Labour and Welfare, Tokyo (in Japanese) Ministry of Social Affairs, Employment

(Ministerie van Sociale Zaken en Werkgelegenheid), the Netherlands (2006) Working conditions act (Act No. 673). Ministry of Social Affairs and Employment, the Netherlands (in Dutch) Muto T, Tomita M, Kikuchi S, Watanabe selleck screening library T (1997) Methods to persuade higher management to invest health promotion programmes in the workplace. Occup Med 47:210–216CrossRef Nauta AP, von Grumbkow J (2001) Factors predicting trust between GPs and Ops. Int J Integr Care 1:e31 Nicholson PJ (2004) Occupational health services in the UK—challenges and opportunities. Occup Med (Lond) 54:147–152CrossRef Oudhoff JP, Timmermans DRM, Knol DL, Bijnen AB, Van der Wal G (2007) Prioritising patients on surgical waiting lists: a conjoint analysis study on the priority judgements of patients, surgeons, occupational physicians, and general

pracitioners. Soc Sci Med 64:1863–1875CrossRef Park H, Ha E, Kim J, Jung H, Paek D (2002) Occupational https://www.selleckchem.com/products/ldk378.html health services for small-scale enterprises in Korea. Ind Health 40:1–6CrossRef Parker D, Brosseau L, Samant Y, Pan W, Xi M, Haugan D, Study Advisory Board (2007) A comparison of the perceptions and beliefs of workers and owners with regard to workplace safety in small metal fabrication businesses. Am J Ind Med 50:999–1009CrossRef Reetoo KN, Harrington JM, Macdonald EB (2005) Required competencies of occupational physicians: a Delphi survey of UK customers. Occup Environ Med 62:406–413CrossRef Russell RM, Maidment SC, Brooke I, Topping 4-Aminobutyrate aminotransferase MD (1998) An introduction to UK schemes to help small firms control health risks from chemicals. Ann Occup Hyg 68:699–704 Terada H, Sone T, Takemura S (2005) A study on actual situation of community industrial physicians for small and medium-sized enterprises and their involvement in community occupational health services. Sangyo Eiseigaku Zasshi 47:259–268 (in Japanese with English abstract)CrossRef Walker

D, Tait R (2004) Health and safety management in small enterprises; an effective low cost approach. Safety Sci 42:69–83CrossRef Weel AN, Plomp HN (2007) Developments in occupational health services in the Netherlands: from a professional to a market regime. Supporting health at work: international perspectives on occupational health services, policy and practice in health and safety, institution of occupational safety and health issue 1 Suppl:87–101″
“Introduction Women report more fatigue than men (Nelson and Burke 2002; Pugliesi 1999; Macintyre et al. 1996), whether this concerns mental fatigue, physical fatigue, sleepiness, feeling tired, or emotional exhaustion (Bakker et al. 2002; Åkerstedt et al. 2004). Women also report sleeping disorders more often than men (Åkerstedt et al. 2004; Peretti-Watel et al. 2009).

Langmuir 2006, 22:10837–10843.CrossRef 26. Mara A, Siwy Z, Trautmann C, Wan J, Kamme F: An asymmetric polymer nanopore for single molecule detection. Nano Lett 2004, 4:497–501.CrossRef 27. Avdoshenko SM, Nozaki D, da Rocha CG, Gonzalez JW, Lee MH, Gutierrez R, Cuniberti G: Dynamic and electronic transport properties selleck inhibitor of DNA translocation through graphene nanopores. Nano Lett 2013, 13:1969–1976.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions LL carried out the experimental design, part of

the experimental work and data analysis, and drafted the manuscript. LZ carried out part of the experimental work. ZN and YC participated in the result discussions. All authors read and approved the final manuscript.”
“Background One-dimensional (1D) ZnO nanostructures have attracted extensive research interests in the past decade due to their versatile application potential in nanooptoelectronics [1], electromechanics [2], and catalysis [3]. It has been found that doping impurities, especially group III elements, such as Al [4], Ga [5], In [6], can significantly enhance the electrical conductivity and influence the optical properties.

In order to generate desirable electrical, optical, and catalytic properties, SB203580 mw 1D ZnO nanostructures have been doped with selected elements. Among these dopants, In is recognized as one of the most efficient elements used to tailor the optoelectronic properties of ZnO [7]. For example, In doping may induce structural defects such as stacking faults [8], twin boundaries [9], and superlattice structures [10], or result in weak localization Morin Hydrate and electron–electron interactions [11], which can significantly affect the electrical and photoluminescence (PL) properties of ZnO nanostructures. On the other hand, it is quite interesting that In doping can change the morphology of ZnO nanowires

(NWs) [12]. There are three typical fast-growth directions ([0001], [10 0], and [11 0]) and ± (0001) polar surfaces in wurtzite ZnO [13]. In general, ZnO NWs grow along [0001] direction. When doped with In, however, they may grow along some other directions, such as the non-polar [01 0] direction [14]. ZnO nanostructures usually have plenty of surface states acting as carrier traps. The existence of such traps is unwanted in catalytic applications, which take advantage of free carriers in the surface region of ZnO nanostructures. In this regard, ZnO nanostructures with large surface-to-volume ratio, high free electron concentration, and low density of surface traps are highly desired. In this work, we demonstrated that such ZnO nanostructures can be achieved via In doping. The In-doped ZnO NWs were grown by one-step vapor transport deposition. The effect of In doping content on the morphology, structure, and optical properties of the NWs has been investigated.

When primers were applied to detect acetylation-associated genes, it was established that the primers designed to target aac (3)-I, aac (3)-II, and aac (3)-III homologues did not generate amplicons. In each of these PCR reactions the positive controls successfully amplified, thus we are satisfied that the lack of amplification products

for our metagenomic sample is a true result. However, a number of distinct aac (6) and aac (3)-VI homologues were detected and were found to resemble genes from a variety of genera, including Acinetobacter, Pseudomonas and Enterobacter (Table 3). The presence of aminoglycoside acetylation genes within these genera has been noted previously [50–53]. The detection of resistance genes resembling those seen in A. baumannii is a concern, as many strains of this species have been shown to exhibit multi-drug resistance Venetoclax mouse [54, 55]. In addition, homologues of genes from Collinsella and Salmonella were also detected. Primers designed to amplify bifunctional aac (6′)-Ie-aph (2′) genes were also employed. Our investigations revealed the

presence of homologues of such genes, resembling those from S. aureus, E. faecium and S. epidermidis, all of which are known sources of these genes [27, 56, 57]. Table 3 Homologues of aminoglycoside resistance genes detected in the human gut microbiota via PCR techniques Accession learn more # Gene description Closest homologue E value % identity aac (6)      

  AAA25680.1 AG 6′-N-acetyltransferase Pseudomonas fluorescens 4 e-48 98 WP_006234103.1 Hypothetical protein Colaer00186 Collinsella aerofaciens 0.0 95 AAS45464.1 6′-N-acetyltransferase A. baumannii 3e-33 75 aac (6′)- Ie-aph (2″)         WP_002304968.1 Phosphotransferase E. faecium 9e-108 100 WP_001028140.1 Acetyltransferase GNAT S. aureus 1e-107 99 WP_001028143.1 Acetyltransferase GNAT S. aureus 1e-107 99 WP_010729367.1 Bifunctional AAC/APH partial sequence E. faecium 5e-106 99 AAX82584.1 Bifunctional AG modifying enzyme Enterococcus faecalis 2e-112 100 WP_002417297.1 6′ AG acetyltransferase E. faecalis 3e-111 97 AFR11868.1 Bifunctional AG 6′-N acetytransferase/2′-AG phosphotransferases S. epidermidis Farnesyltransferase 1e-43 99 AFM29914.1 Gentamycin resistance protein Enterococcus sp. 7e-45 97 aph (2″) Id         3SG8_A Chain A crystal structure AG 2′ phosphotransferases E. casseliflavus 1e-110 98 3N4T_A Aph2″ chain a E. casseliflavus 2e-110 99 AAT77696.1 AG modifying enzyme E. faecium 1e-68 94 Aph (2″)-Ic         3TDVA AG phosphotransferase Enterococcus gallinarum 2e-83 97 ant (2″) Ia         YP_005176240.1 AG 2′–O-adenyltransferase Pasturella mutocida 2e-97 100 WP_000314377.1 2′ AG nucleotidlytransferase A. baumannii 3e-94 99 WP_000946493.1 2′ AG A. baumannii 1e-94 99 ACJ47203.1 AG adenyltransferase E. coli 6e-94 99 ACA48663.14 AG adenyltransferase Morganella morganii 2e-96 99 aac (3)-VI         AAA16194.

(b) The second sentence of the sixth paragraph (right column, p. 1019) should have been: “In addition, a careful examination of spectroscopic data obtained by different techniques and an exploration of all spectroscopic characteristics (not only special features) does not support the existence of separate crystalline phases different from those of apatite, even in the samples of bone

from the youngest animals.”   (c) The sentence beginning on line 24 of the sixth paragraph (right column, p. 1019) should have been: “As already noted, these ions are not compatible with the formation of OCP crystals, and to date, no carbonate-containing OCP crystals or other non-apatitic phases have been detected.”   (d) The first sentence of the penultimate paragraph (left

column, p. 1020) AZD2014 ic50 should have been: “We also note the following reservations we have about HSP signaling pathway the conclusions reached by Mahamid et al. [69]: The FTIR band at 961 cm−1 is characteristic of apatite and not carbonated apatite; this band is due to phosphate ions in any HPO 4 2− or carbonate-containing apatite.””
“Dear Editors, In postmenopausal women, whether supplementation of calcium reduces bone loss or not is a contentious issue. The latest analysis by Professor Nordin [1] is a valiant effort to resolve the issue. By using a meta-analytic Beta adrenergic receptor kinase approach, Professor Nordin concludes that daily calcium supplement of 100 mg could protect against bone loss for up to 4 years. This conclusion appears to be based on the mean difference in the rate of change in BMD between the control and treated (calcium supplementation) groups. However, a close reading of the analysis reveals a number of methodological shortcomings that could potentially compromise the author’s

conclusion. It is well known that the rate of change in BMD varies remarkably among individuals, with the standard deviation being 2–4 times higher than the average [2, 3]. This heterogeneity is observed not just in nontreated populations, but also in randomized controlled clinical trials [4], where it ranged between 2.1% and 5%. However, in the present paper, it is reported that the standard deviation of BMD change was less than 1% for both control and treated groups. This low variability is likely due to the way the data from individual studies were analyzed. There are two important sources of variation in the rates of change in BMD: between-study and within-study variation. It is critically important to weight the within study variation, because studies with large variance (i.e. less consistent effect) should have less weight than studies with small variance (i.e. more consistent effect).