16,7%, p = 0,71). As variáveis idade, sexo, tipo de residência ou realização de colonoscopia prévia não se mostraram como fatores com influência na qualidade da preparação intestinal. Existem poucos estudos acerca

do impacto que um ensino personalizado ao doente poderá ter na melhoria da preparação para colonoscopia. Um estudo americano de 20095 concluiu que a estratégia interventiva educacional ao doente não provocou melhoria global na qualidade da preparação intestinal, mas o tipo de alimentação ingerida nas 24 horas prévias ao exame (sólido vs. líquido) e o tempo desde a última refeição sólida (> 24 horas vs. < 24 horas) tiveram impacto positivo (p = 0,04 e p = 0,03, respetivamente). No nosso estudo verificámos uma melhoria global da qualidade da preparação nos doentes submetidos a ensino Seliciclib chemical structure (limpeza intestinal boa ou excelente: 58,6% vs. 38,8%, p = 0,03), e uma menor percentagem de qualidade

má ou inadequada (16,4% no grupo «controlo» e 1,7% no grupo «intervenção», p = 0,005). A percentagem global de má preparação foi de 9,6%, valor inferior ao que geralmente é descrito na literatura2, 3 and 4, mas os critérios para definir a qualidade da preparação não são iguais entre os estudos. A melhoria na qualidade da limpeza intestinal verificada com o ensino é obtida através de uma intervenção direta no doente aumentando a sua colaboração, adaptada às selleckchem suas capacidades intelectuais e antecedentes pessoais, e que atua sobre as várias vertentes do exame: o procedimento, a preparação e a dieta. Está definido que deve ser efetuada uma dieta pobre em fibras nos dias que precedem a colonoscopia

e uma dieta líquida na véspera7, 9, 12 and 13, sendo um conteúdo alto de resíduos na dieta um fator preditivo independente 3-oxoacyl-(acyl-carrier-protein) reductase de má preparação intestinal8. No entanto, não há normas definidas quanto à duração e ao tipo de alimentos, e a adesão do doente a este tipo de dieta pode ser baixa9. No nosso estudo, os doentes efetuaram uma dieta pobre em resíduos previamente à colonoscopia, com duração variável consoante os antecedentes de cirurgia abdominal e obstipação, e personalizada ao gosto do doente com seleção do tipo de alimentos. Podemos admitir que não só o baixo conteúdo em fibras como também a duração e o tipo de alimentos contribuíram para a melhoria da qualidade da preparação intestinal, já que estas medidas constituem as principais diferenças na intervenção entre os 2 grupos. Há alguns subgrupos de doentes que poderão beneficiar mais com esta estratégia. A obstipação crónica é um fator preditivo de preparação intestinal inadequada14 and 15, e uma intervenção personalizada, ao nível da duração da dieta antes da colonoscopia, parece levar a uma melhoria da qualidade da preparação (p = 0,04).

, 2008 and Syed and Leal, 2009), decanal, undecanal, phenylacetaldehyde, furfural, trans-2-methyl-2-butenal, benzaldehyde, phenol, 2-methylphenol, 3-methylphenol, Angiogenesis inhibitor 4-methylphenol, 4-ethylphenol, 3,5-dimethylphenol, 2,3-dimethylphenol, 2-methoxy-4-propylphenol, guaiacol, indole, 3-methylindole (=skatole)

( Blackwell et al., 1993, Leal et al., 2008, Millar et al., 1992 and Olagbemiro et al., 2004), butylamine, heptylamine, octylamine, trimethylamine ( Leal et al., 2008), nonanoic acid, (±)-lactic acid, geraniol, nerol, geranylacetone ( Logan et al., 2009 and Logan et al., 2010), trans-p-menthane-3,8-diol, cis-p-menthane-3,8-diol ( Paluch et al., 2010), geranyl acetate, (±)-linalool ( Choi et al., 2002), (−)-fenchone, (+)-fenchone, (±)-thujone, linalool oxide, (±)-eucalyptol, eugenol ( Kafle and Shih, 2013), and (±)-citronellal ( Paluch et al., 2010). Prior

to publication of the Cx. quinquefasciatus genome ( Arensburger et al., 2010), we identified and de-orphanized two ORs from the Southern house mosquito. We named them CquiOR2 ( Pelletier et al., 2010) and CquiOR10 ( Hughes et al., 2010) based on shared high amino acid identity with AgamOR2/AaegOR2 and AgamOR10/AaegOR10 from the mosquitoes An. gambiae and Aedes (Stegomyia) aegypti, respectively. RT-PCR analysis showed that CquiOR2 and CquiOR10 genes are expressed exclusively in olfactory tissues. While neither was detected in non-olfactory tissues from adult females, CquiOR2 was expressed only in selleck inhibitor antennae, whereas CquiOR10 was expressed mainly in antennae and secondarily in maxillary palps ( Pelletier et al., 2010). We then demonstrated with the Xenopus oocyte recording system that CquiOR2 responded to various compounds with indole being the best ligand ( Pelletier et al., 2010), whereas CquiOR10 was narrowly tuned to the oviposition attractant skatole ( Hughes et al., 2010). CquiOR2 and CquiOR10 shared high amino acid

identity with two annotated ORs in the genome of Cx. Resveratrol quinquefasciatus: CquiOR121 (VectorBase, CPIJ802644; formerly CPIJ014392) and CquiOR21 (VectorBase, CPIJ801844; formerly CPIJ002479; previously named CqOR2 in VectorBase), respectively. CquiOR2 and CquiOR121 differ in 4 residues, Glu- vs Gln-89, Phe- vs Val-171, Lys- vs Glu-235, and Asp- vs Glu-301. They may be isoforms caused by single nucleotide polymorphism (SNPs) differences. Cx. quinquefasciatus and related Culexpipiens complex mosquitoes have a very high densities of SNPs, in fact more than any other mosquito thus far studied ( Lee et al., 2012). It is worth mentioning that the genome was sequenced from the Johannesburg strain ( Arensburger et al., 2010), whereas we cloned the genes ( Hughes et al., 2010 and Pelletier et al.

Dose response curves were measured in triplicate, and controls (1 nM dihydrotestosterone (DHT) Selleckchem Roscovitine and 0.1% ethanol, respectively) were repeated 6-fold. Measurement of luciferase activity was performed in cellular crude extracts using a Synergy HT plate reader from BioTek (Bad Friedrichshall, Germany). Cells were lysed in situ using 50 μl of lysis buffer (0.1 M tris–acetate, 2 mM EDTA, and 1% triton-x, pH 7.8), shaking the plate moderately for 20 min at room temperature. Following cellular lysis 150 μl

of luciferase buffer (25 mM glycylglycine, 15 mM MgCl2 and 4 mM EGTA, 1 mM DTT, 1 mM ATP, pH 7.8) and 50 μl of luciferin solution (25 mM glycylglycine, 15 mM MgCl2 and 4 mM EGTA, 0.2 mM luciferin, pH 7.8) were added automatically to each well in order to measure luminescence. All values were corrected for the mean of the negative control and then related to the positive control which was set to 100%. Cell line HeLa9903 was obtained from the JCRB (JCRB-No. 1318). These cells contain stable expression constructs for human ERα and firefly luciferase, respectively. The selleck products latter is under transcriptional control of five ERE promoter elements from the vitellogenin gene. The transcription of ERα was confirmed by RT-PCR, as was the absence of AR-transcripts (Fig. S1). The assay was performed according

to the OECD test guideline TG455 (OECD, 2009) as follows. Cells were cultivated in phenol red free MEM containing 10% (v/v) of charcoal stripped FCS at 37 °C in an atmosphere with 5% CO2. For the actual assay cells were seeded into white 96-well polystyrene plates at a concentration of 104 cells per 100 μl and well (Costar/Corning, Amsterdam, Netherlands). Test substances were added 3 h after seeding by adding 50 μl of triple concentrated substance stocks to each well. As before dose response curves for treated samples were measured ASK1 in triplicate, while controls (1 nM E2 or 0.1% ethanol, respectively) were repeated 6-fold. After 24 h of stimulation, cells were washed with PBS and then lysed using 50 μl

of lysis buffer and moderate shaking for 20 min at room temperature. Subsequent measurement of luciferase activity was performed analogous to the aforedescribed androgen reporter gene assay. All values were corrected for the mean of the negative controls and then related to the positive controls set as 100%. Cell line MCF-7 was obtained from the ATCC (ATCC-No. HTB-22) and checked with RT-PCR for transcription of ER, AR, GPR30 and AhR (Fig. S1). Cells were routinely passaged in RPMI 1640 medium containing 10% FCS (v/v), 100 U/ml Penicillin and 100 μg/ml streptomycin and grown at 37 °C in an atmosphere with 5% CO2. Prior to the actual assays the cells were transferred into hormone-free medium (phenol red free RPMI 1640 with 5% of charcoal stripped FCS).

, 2007 and Karlson et al., 2008). PTJC=Prediction of Tender Joint Count=−26.72+3.243∗[YKL-40]1/10−11.97*[EGF]1/10+15.72∗[IL-6]1/10+0.4594∗[Leptin]1/10+3.881∗[SAA]1/10+0.7388∗[TNF-RI]1/10−0.2557∗[VCAM-1]1/10+0.7003∗[VEGF-A]1/10 PSJC=Prediction of Swollen Joint Count=−26.63+3.232∗[YKL-40]1/10−11.93∗[EGF]1/10+15.67∗[IL-6]1/10+0.4578∗[Leptin]1/10+3.868∗[SAA]1/10+0.7363∗[TNF-RI]1/10−0.2548∗[VCAM-1]1/10+0.6979∗[VEGF-A]1/10

MG-132 mw PPGS=Prediction of Patient Global Score=−13.489+5.474∗[IL-6]1/10+0.486∗[SAA]1/10+2.246∗[MMP-1]1/10+1.684∗[Leptin]1/10+4.14∗[TNF-RI]1/10+2.292∗[VEGF-A]1/10–1.898∗[EGF]1/10+0.028∗[MMP-3]1/10–2.892∗[VCAM-1]1/10–0.506∗[Resistin]1/10 MBDA score=round(max(min((.56∗sqrt(max(PTJC,0))+.28∗sqrt(max(PSJC,0))+.14∗PPGS+.36∗log(CRP/10^6+1))∗10.53+1,100),1))MBDA score=roundmax(min((.56∗sqrt(max(PTJC,0))+.28∗sqrt(max(PSJC,0))+.14∗PPGS+.36∗log(CRP/10^6+1))∗10.53+1,100),1)

All concentration values except that of CRP are X1/10 transformed prior to use in the algorithm. MBDA algorithm scores are integers from 1 to 100, with disease activity thresholds designed to be equivalent Copanlisib to thresholds from DAS28CRP: • MBDA algorithm scores ≤ 29 are considered low disease activity. All autoantibody assays exhibited less than 10% difference (median difference) between the two sample types (Table 3), well within the Food and Drug Administration suggested specification at ± 15% for accuracy (FDA, 2001). Tolmetin All analyses for autoantibodies were calculated on raw signals in antibody biomarker measurements. An additional more stringent analysis compared the correlation coefficient and slope of linear regression. In comparison of plasma and serum matched sample sets, the correlation was 0.99 (0.98 to 1.00) with a slope of approximately

1.00, indicating little or no difference in quantitation of autoantibody signals in serum vs. plasma samples. For protein biomarkers of matched plasma and serum samples, only 67% of the biomarkers were highly correlated achieving correlation coefficients of 0.95 (range 0.33–1.00) (Table 3). The protein concentrations had a systematic shift with the slope of most markers being less than 1.00, indicating serum concentrations were measured higher for most biomarkers. The plasma EGF concentrations were not correlated with matched serum EGF concentrations (correlation coefficient of 0.33). As shown in Fig. 1A, 5 out of 12 protein biomarkers (VCAM-1, EGF, VEGF-A, MMP1 and resistin) had shifts > 15% in the median % difference in concentration across the 32 patient samples. Aside from leptin and MMP-1, median protein concentrations in plasma were lower than those in serum. While the median change for MMP-1 showed significantly greater concentrations in plasma over serum (Fig. 1A), the individual subjects in this study provided mixed results, with 12 subjects’ plasma showing lower MMP-1 concentrations and 20 subjects with greater MMP-1 concentrations.

29, 30 and 31 CE yielded a 7% increase in the detection of any dysplasia.31 Compared with white-light colonoscopy with random biopsies, the likelihood to detect any dysplasia with CE and targeted biopsies was 8.9-fold greater, and 5.2-fold greater for detecting nonpolypoid dysplasia. In a Mainz study of 165 patients with long-standing UC who were randomized to undergo standard colonoscopy using white light versus CE (0.1% methylene blue), significantly more intraepithelial neoplasms were detected in the CE group (32 vs 10; P = .003). CE detected more intraepithelial

neoplasms in “flat mucosa” than white-light endoscopy (24 vs 4; P = .0007), and more invasive cancers (3 vs 1). 26 In these studies, colonoscopies were find more performed by dedicated colonoscopists with expertise in multimodal imaging, and under controlled circumstances (ie, clinical trials), and may preclude Veliparib supplier generalizability. Recognition of the nonpolypoid dysplasia in a real-world environment remains challenging and requires additional training. In a study conducted at Maastricht University Medical Center, where the

endoscopists have been trained on the recognition of nonpolypoid neoplasms,32 the overall detection rate of sporadic NP-CRNs (defined as lesions of which the height was less than half of the diameter) was 5.7% (diagnostic subgroup, 4.7%; screening subgroup, 4.5%; surveillance subgroup, 15.6%).33 The learning-curve in the detection Ergoloid of NP-CRNs is, however, tedious, with at least 600 colonoscopies being required to achieve a detection rate of at least 4.5%.34 It is highly likely that missed lesions have a major contribution to the development of interval CRCs in patients with IBD, although this needs further investigation. The current data highlight the importance of vigilant inspection and a thorough phenotyping of lesions identified at colonoscopy, including subtle erosions, shallow ulcerations, and their relationship with inflammation

or strictures. Such exquisite detail may improve the understanding of the link between inflammation, the occurrence of dysplasia, and interval CRCs. High-quality videos/photodocumentation obtained in a standardized fashion facilitates this process. Challenging cases should be performed by expert endoscopists. Endoscopic resection of neoplasms in the context of colitis is clearly fraught with difficulties because of the presence of inflammation and scarring. Such conditions challenge the accurate detection, clear demarcation, and lifting of the lesions. Studies examining the diagnostic yield of CE during surveillance for IBD provided, however, limited information about the effectiveness of the endoscopic resection, which requires further investigation.

Although the starting activities of such designed enzymes is low, random mutagenesis at the active site and at more distant locations can be used to improve the activity [ 52••]. To explore the structural basis of these changes and to augment the activity of the designer aldolase, further rounds of directed evolution were carried out and X-ray crystal structures of the enzyme in complex with a mechanism-based inhibitor were solved after each stage of evolution. In the initial designer enzyme (RA95.0) the inhibitor reacts covalently

with Lys210 as was intended for the designer enzyme. However, during the evolution of increased activity (variant RA95.5) a new lysine was introduced PI3K inhibitor into the active site (Lys83) during cassette mutagenesis and unexpectedly RA95.5 is modified twice by the mechanism-based inhibitor — once at Lys210, as in RA95.0, and once at the newly introduced Lys83 ( Figure 2). After further rounds of error prone PCR variant RA95.5-5 was constructed which contained additional mutations and which was >20-fold more efficient than RA95.5 and >1700-fold more active than the original in silico design.

Structurally this variant showed further modulation of loops of the protein, but interestingly was only modified by the inhibitor at Lys83, implying that this new binding site is more evolvable than the original GDC 0199 designer site. Subjecting this evolved retro-aldolase to further error prone PCR produced an enzyme with activity approaching that of a natural aldolase, notable for an artificial enzyme. This work demonstrates how

powerful the combination of computational and traditional methods can be and also allows insight into the mechanisms that lead to enhanced catalytic efficiency [ 52••]. The synthetic utility of aldolase enzymes may be substantially increased using protein engineering approaches. Complementary approaches have been exploited to improve the properties of aldolases including their stability, substrate scope and stereoselectivity. Excitingly, the increased understanding of the function of aldolase variants, together with computational approaches, can help focus protein engineering experiments on specific, functionally important residues. Such approaches can improve the efficiency of searching before within sequence space, enabling more rapid discovery of enzymes with the required synthetically valuable properties. The future use of these important enzymes looks bright with the ability to link engineered aldolases with other enzymes in novel constructed pathways and organisms opening the way to their increased use in synthetic biology to more easily produce valuable but useful complex compounds. Papers of particular interest, published within the review period, have been highlighted as: of special interest of outstanding interest CLW is supported by a studentship from the BBSRC (BB/F01614X/1).

Instead, the transmit coil is a quadrature double-loop design, with appropriate overlap between the two loops to minimize the mutual inductance [19]. The diameter of each loop is 20 cm with an overlap of ∼3 cm. Each loop is segmented into eight separate sections with 3.9 pF non-magnetic capacitors (American Technical Ceramics, Series B, Huntington Station, NY) and one 1–30 pF variable capacitor (Johansson, Camarillo, CA) for fine tuning. Balanced impedance matching was achieved using one 1–40 pF www.selleckchem.com/products/icg-001.html variable and one fixed 33 pF capacitor. A 1-cm thick foam padding was placed between the coil and the subject. Each loop was impedance matched at 298.1 MHz with an S11 measurement

of lower than −20 dB when the coil was placed on the subject. The isolation APO866 manufacturer under loaded conditions between each channel was between −18 and −24 dB for each subject studied. The unloaded and loaded Q values were 150 and 20, respectively. A detuning voltage of +12 V is supplied from the spectrometer, and is used to drive a conventional active PIN-diode decoupling circuit [20].

The receive coil is an eight-element array, shown schematically in Fig. 1, with each element being octagonal in shape and split by five 3.9 pF fixed value series capacitors and one 1–30 pF variable capacitor for fine tuning. Balanced impedance matching, an LC lattice balun, and small “figure-8 cable traps” were placed in front of each element of the array. The more common cable-traps are loops of coaxial-cable wound to make an inductor with a capacitor across the gap in the shield to resonate the shield. This configuration produces an extra B-field which can either produce unwanted signal or interfere with the main coil if it is placed very close. By wrapping the coaxial-cable into a figure-eight rather than single loop, any extraneous B-field is reduced. Each element in the coil is ∼14 cm wide in the z-dimension, and is overlapped by ∼2 cm in this direction. The Cytidine deaminase total length of the array is 91 cm. The coaxial-cables (length ∼1 m) attached to each element of the array are grounded

together at the coil, and again at a distance approximately one-quarter wavelength away. This significantly reduces the effects of the environment within the magnet interacting with the RF cables. A 1-cm thick piece of foam was placed on top of the RF coil, on which the subject lies. Each element was impedance matched to less than −20 dB on the S11 measurement, with nearest neighbor coil isolation greater than −15 dB, and next-nearest neighbour greater than −25 dB, when loaded. A detuning voltage of −3.6 V is supplied for each channel from the spectrometer, and is used to power two active PIN-diode decoupling circuits [20] across the variable tuning and matching capacitors. Additional passive cross-diode circuits are used for each coil.

17 ± 1.57, P < 0.0001) that was not observed with IL-6 treatment, while IL-6 increased SOCS3 expression (3.88 ± 0.59, Selleck 17-AAG P = 0.0002), but BMP6 did not. The BMP receptor antagonist, dorsomorphin, used as a negative control, inhibited ID3 expression (0.48 ± 0.16, P < 0.0001). The HDAC inhibitor, vorinostat, which was one of the most potent Hepcidin stimulating chemicals identified in the screen, produced a particularly strong increase

in Hepcidin (15.09 ± 0.55, p < 0.0001) and ID3 expression (10.3 ± 0.33, P < 0.0001). The majority of chemicals that significantly upregulated Hepcidin transcript levels significantly upregulated ID3, with the exception of daunorubicin, ethacridine, and 9-aminoacridine, which either decreased or did not

affect ID3 expression ( Fig. 2B). Interestingly, the Hepcidin agonists that did not upregulate ID3, did upregulate SOCS3, consistent with Stat3 pathway activation ( Fig. 2C). Thus the Hepcidin agonists can be divided into three classes: (1) upregulators of BMP signaling only, (2) upregulators of Stat3 signaling only, and (3) upregulators of both pathways ( Fig. 2D). We were particularly interested in the kinase Z-VAD-FMK price inhibitors, GTP 14564, AG1296, and SU6668, since they each affect growth factor dependent signaling, which has previously been shown to affect Hepcidin expression  [24]. GTP 14564 inhibits FLT3, c-Fms, c-Kit, and PDGFRβ [25], while AG1296 impairs signaling by both PDGF-α and β receptors and by c-Kit [26]. SU6668 has broad effects against receptor tyrosine kinases and inhibits VEGF, FGF, and PDGF receptors [27]. To validate the initial classification of these compounds by ID3 and SOCS3 expression ( Figs. 2B–D), we evaluated these chemicals for their effects on transcription of an additional BMP-dependent gene, ID1 [20], [21] and [22], and additional Stat3-dependent genes [23] and [18], IL6 receptor (IL6R) and VEGFA. We found that GTP 14564 and SU6668 each Montelukast Sodium significantly upregulated expression of ID1,

as well as IL6R and VEGFA ( Figs. 3A–C). Although AG1296 did not significantly increase expression of ID1, it did significantly increase transcript levels of BMP and Stat3-dependent genes, including ID3 ( Fig. 2B), SOCS3 ( Fig. 2C), and VEGFA ( Fig. 3C). Thus it appears that these growth factor receptor tyrosine kinase inhibitors upregulate both the BMP and Stat3 signaling pathways. To assess the effects of growth factors on Hepcidin promoter activity, we treated the Hepcidin-Luciferase HepG2 cells with EGF 150 ng/ml, FGF 200 ng/ml, PDGF 50 ng/ml, VEGF 150 ng/ml, or FLT3 150 ng/ml for 24 h in the presence or absence of the tyrosine kinase inhibitors, AG1296 (5 μM) or GTP 14564 (5 μM) ( Fig. 3D). We found that each of these proteins significantly reduced baseline Hepcidin promoter activity.

Taking these issues into account is a decision with a long-term view: any effect of the sum of one’s own healthy choices or the society’s sustainable food choices will show at a later point in time (as good health in later age, or environmental resources well-preserved for the next generation). Therefore, it is most likely those consumers who are already able to fulfil the more immediate needs and wants [2], who can afford to fulfil their 3-MA cost need to secure health in the long run or express themselves in ethical choices. Because of these reasons, both issues of health and sustainability are often assumed to be received best by a similar target group, as has also been shown in consumer

segmentation research 33•• and 41, and both issues might also be communicated in a similar way. One explanation for why organic food is regarded as more healthy by consumers is that it is perceived to be less processed, more natural and expected to be free from pesticides or dubious (in consumer perception) substances and technologies used in production and processing, such as preservatives, genetic LDK378 solubility dmso modification and nanotechnologies [42]. Food consumers assume natural products are healthier [43], and many consumers show modern health worries, which are concerns about risks related to modern technologies [44]. However, apart from that, one can also assume that consumers think in a

more holistic and ecological approach, acknowledging interconnectivity: If a consumer prefers a seemingly more environmentally friendly product out of health motives, it might be because she or he is aware of environmental pollution and degradation affecting human health in the end. In this thinking, there is not necessarily a distinction Liothyronine Sodium possible between a self-centred health concern and an altruistic concern for sustainability, as both are connected. Furthermore, it has been argued that even though the major driver might be altruistic concern,

consumers might report more strongly on self-centred motives in order to show and justify rationality of their choice [45]. Therefore, there might be a strong link, instead of a divide, between health and sustainability from a consumer point of view. This is exemplified by certain consumer trend groups such as the LOHAs (lifestyle of health and sustainability, [46]) or the voluntary simplifiers or downshifters, given that they seek to combine healthy with sustainable lifestyles or seek simpler lifestyles and consumption for the sake of a more healthful, holistic and non-materialistic, but spiritually rich lifestyle [47]. Interestingly, reducing working hours, as advocated by downshifters, has been identified as potentially reducing resource intensity of lifestyles [19••]. Furthermore, it has been found that those consumers interested in ‘alternative’ foods also seem to eat healthier [48].

For the reader’s convenience, the correct figure is reproduced here along with its legend. “
“On the cover, the incorrect cover legend was used. For the reader’s convenience, the correct legend is reproduced

here along with the figure. Figure options Download full-size image Download high-quality image (254 K) Download as PowerPoint slide Skeleton pain is transmitted by a specific subset of sensory nerve fibers. Bone is preferentially Obeticholic Acid cell line innervated by peptidergic-rich C-nerve fibers (CGRP+ nerve fibers; in green) and myelinated Aδ/β nerve fibers (NF200+ nerve fibers; in red) but not peptidergic-poor C-nerve fibers which are abundantly present in skin. This restricted innervation presents a therapeutic opportunity for treating skeletal pain. Confocal images from periosteal whole preparations were acquired and overlapped on a three dimensional image of the mouse femur obtained by microcomputed tomography. In this illustration only the sensory innervation of the periosteum is shown. Images were rendered courtesy of Marvin Landis (University Information Technology Services, University of Arizona). Figure from “A phenotypically restricted set of

primary afferent nerve fibers innervate the bone versus skin: therapeutic opportunity for treating skeletal pain” by Jimenez-Andrade et al. found page of 306–313 of this issue. “
“In the author line the name of T. John Martin was accidentally omitted. The correct author line appears above.

“
“The following abstracts were mistakenly not included in the Vasopressin Receptor “2nd Joint Meeting Histone Methyltransferase inhibitor of the International Bone and Mineral Society and the Australian and New Zealand Bone and Mineral Society” issue. For the reader’s convenience, the abstracts have been reproduced in this issue. Costa JL, Watson M, Callon KE, Hochgeschwender U, Cornish J. Analysis of bone in POMC knockout mice. Bone; 10.1016/j.bone.2009.12.012. Chhana A, Callon KE, Pool B, Cornish J, Dalbeth N. Mechanisms of erosive gout: monosodium urate monohydrate crystals reduce osteoblast viability, Bone; 10.1016/j.bone.2009.12.013. Xia Z, Locklin RM, Wang X, Bava U, Cornish J, Hulley PA. Development of three-dimensional cultures for assessment of cell proliferation and osteogenic differentiation in vitro, Bone; 10.1016/j.bone.2009.12.014. “
“Figure options Download full-size image Download high-quality image (221 K) Download as PowerPoint slide Etsuro Ogata was born on January 5, 1932, and passed away on November 1, 2009, after a long illness. A scientist and an academic of great national and international distinction, he made notable contributions to the field of calciotropic hormones and bone as well as cancer-associated endocrine and metabolic disorders. His published works in those areas provide a substantial body of high-quality science of real impact, and he was indeed a major scientific figure in mineral metabolism and bone as well as in endocrinology.