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991.
SlyD from Escherichia coli is a peptidyl–prolyl cis–trans isomerase involved in [Ni–Fe] hydrogenase metallocentre assembly in bacteria. We present here the backbone and side chain
assignments for E. coli SlyD. 相似文献
992.
Mary‐Elizabeth Patti Sander M. Houten Antonio C. Bianco Raquel Bernier P. Reed Larsen Jens J. Holst Michael K. Badman Eleftheria Maratos‐Flier Edward C. Mun Jussi Pihlajamaki Johan Auwerx Allison B. Goldfine 《Obesity (Silver Spring, Md.)》2009,17(9):1671-1677
The multifactorial mechanisms promoting weight loss and improved metabolism following Roux‐en‐Y gastric bypass (GB) surgery remain incompletely understood. Recent rodent studies suggest that bile acids can mediate energy homeostasis by activating the G‐protein coupled receptor TGR5 and the type 2 thyroid hormone deiodinase. Altered gastrointestinal anatomy following GB could affect enterohepatic recirculation of bile acids. We assessed whether circulating bile acid concentrations differ in patients who previously underwent GB, which might then contribute to improved metabolic homeostasis. We performed cross‐sectional analysis of fasting serum bile acid composition and both fasting and post‐meal metabolic variables, in three subject groups: (i) post‐GB surgery (n = 9), (ii) without GB matched to preoperative BMI of the index cohort (n = 5), and (iii) without GB matched to current BMI of the index cohort (n = 10). Total serum bile acid concentrations were higher in GB (8.90 ± 4.84 µmol/l) than in both overweight (3.59 ± 1.95, P = 0.005, Ov) and severely obese (3.86 ± 1.51, P = 0.045, MOb). Bile acid subfractions taurochenodeoxycholic, taurodeoxycholic, glycocholic, glycochenodeoxycholic, and glycodeoxycholic acids were all significantly higher in GB compared to Ov (P < 0.05). Total bile acids were inversely correlated with 2‐h post‐meal glucose (r = ?0.59, P < 0.003) and fasting triglycerides (r = ?0.40, P = 0.05), and positively correlated with adiponectin (r = ?0.48, P < 0.02) and peak glucagon‐like peptide‐1 (GLP‐1) (r = 0.58, P < 0.003). Total bile acids strongly correlated inversely with thyrotropic hormone (TSH) (r = ?0.57, P = 0.004). Together, our data suggest that altered bile acid levels and composition may contribute to improved glucose and lipid metabolism in patients who have had GB. 相似文献
993.
L. Pilloni P. Bianco C. Manieli G. Senes P. Coni L. Atzori N. Aste G. Faa 《European journal of histochemistry : EJH》2009,53(2)
Basal cell carcinoma (BCC) is a very common malignant skin tumor that rarely metastatizes, but is often locally aggressive. Several factors, like large size (more than 3 cm), exposure to ultraviolet rays, histological variants, level of infiltration and perineural or perivascular invasion, are associated with a more aggressive clinical course. These morphological features seem to be more determinant in mideface localized BCC, which frequently show a significantly higher recurrence rate. An immunohistochemical profile, characterized by reactivity of tumor cells for p53, Ki67 and alpha-SMA has been associated with a more aggressive behaviour in large BCCs. The aim of this study was to verify if also little (<3 cm) basal cell carcinomas can express immunohistochemical markers typical for an aggressive behaviour.Basal cell carcinoma (BCC) is a very common malignant skin tumor that rarely metastatizes, even If Is often locally aggressive. Several factors, like large size (more than 3 cm), face localization, exposure to ultraviolet rays, histological variants, infiltration level and perineural or perivascular invasion, are associated with a more aggressive clinical course. In particular, the incidence of metastasis and/or death correlates with tumors greater than 3 cm in diameter in which setting patients are said to have 1–2 % risk of metastases that increases to 20–25% in lesions greater than 5 cm and to 50% in lesions greater than 10 cm in diameter (Snow et al., 1994). Histologically morpheiform, keratotic types and infiltrative growth of BCC are also considered features of the most aggressive course (Crowson, 2006). This can be explained by the fact that both the superficial and nodular variants of BCC are surrounded by a continuous basement membrane zone comprising collagens type IV and V admixed with laminin, while the aggressive growth variants (i.e. morpheiform, metatypical, and infiltrative growth subtypes) manifest the absence of basement membrane (Barsky et al., 1987).The molecular markers which characterize aggressive BCC include: increased expression of stromolysin (MMP-3) and collagenase-1 (MMP-1) (Cribier et al., 2001), decreased expression of syndecan-1 proteoglycan (Bayer-Garner et al., 2000) and of anti-apoptotic protein bcl-2 (Ramdial et al., 2000; Staibano et al., 2001).C-ras , c-fos (Urabe et al., 1994; Van der Schroeff et al., 1990) and p53 tumor supressor gene mutations (Auepemikiate et al., 2002) are indicative of an aggressive course.Focusing upon bcl-2 and p53 expression in BCC, there have been numerous studies documenting the utility of bcl-2 as a marker of favourable clinical behaviour while p53 expression may be a feature of a more aggressive outcome (Ramdial et al., 2000; Staibano et al., 2001; Bozdogan et al., 2002).An increased expression of cytoskeletal microfilaments like α–smooth muscle actin, frequently found in invasive BCC subtypes (Jones JCR et al., 1989), may explain an enhanced tumor mobility and deep tissue invasion through the stroma. (Cristian et al., 2001; Law et al., 2003). The aim of this preliminary study was to verify if also little (<3 cm) basal cell carcinomas may express aggressive immunohistochemical markers like p53, Ki67 and alpha-SMA. We used 31 excisional BCCs with tumor size less than 2 cm (ranging from 2 up to 20 mm) and with different skin localization (19 in the face, 6 in the trunk and 6 in the body extremities). All cases were immunostained for p53, BCL2, Ki67 and alpha-smooth muscle actin (α-SMA) (Age Sex Location Hystotype Max.Dim Depth Ulc Ess Inf p53 Bcl-2 Ki67 AML 1 61 M Extr Keratotic 10×8 1 No +++ URD +++ + + - 2 61 M Face Adenoid 10×9 4 No + URD +++ - - - 3 64 M Extr Sup mult 11×13 0.8 No + DRD + - - - 4 73 M Face Nodular 10×8 2 Yes + DRD +++ + ++ +++ 5 84 M Face Nodular 9×12 2 Yes + DRD - - - - 6 84 M Face Adenoid 5 0.8 No + URD +++ - - - 7 84 M Extr Nodular 13×10 3 No + DRD +++ + + - 8 52 F Face Nodular 4 0.8 No + URD + + + - 9 76 F Face Adenoid 10×4 4 No + DRD +++ - ++ - 10 77 F Face Morph 8×6 1 Yes +++ DRD +++ - - - 11 86 M Face Morph 8 1 Yes + DRD +++ - + + 12 63 F Face Adenoid 4 1 No + URD ++ + + + 13 76 F Face Nodular 7 1.5 No + DRD +++ + ++ - 14 84 M Face Nodular 11 4 Yes +++ DRD + - - + 15 63 F Face Keratotic 10×6 1.8 No ++ DRD - + ++ - 16 68 F Trunk Sup mult 10×6 0.7 No ++ URD + + - - 17 67 M Face Sup mult 12×6 0.4 No + URD + - + - 18 67 M Extr Sup mult 4×3 0.3 No + URD + +++ + - 19 32 F Extr Sup mult 1×3 0.4 No + URD + + + - 20 45 M Trunk Nodular 7×5 2 Yes +++ URD + + + - 21 62 M Trunk Sup mult 11×7 0.9 No ++ URD - ++ - ++ 22 65 M Trunk Adenoid 7×6 1.5 No + URD +++ + + - 23 72 M Trunk Nodular 12×6 1 No + URD +++ - + + 24 86 F Face Keratotic 20×11 3.1 No ++ DRD + + + - 25 85 M Face Nodular 0.5 1.3 No ++ DRD ++ + + - 26 74 F Extr Nodular 4×4 0.9 No + URD - - + - 27 71 M Face Nodular 6×12 1.7 No + DRD - - + - 28 64 F Trunk Sup mult 1.3×1.5 0.4 No ++ URD +++ - - - 29 78 F Face Nodular 4×3 1.5 No ++ DRD ++ + - +++ 30 80 M Face Keratotic 4×4 1.6 Yes + DRD - - + +++