46,521 research outputs found
Stellar Cluster Member Data
No full textTab-separated ASCII machine readable tables of the stellar data for individual cluster members used in the calculation of the mean cluster properties in Zucker et al. 2022 (DOI: 10.1038/s41586-021-04286-5).
Data columns are as follows:
(1) source_id: Gaia EDR3 source ID
(2) l: Galactic Longitude (deg)
(3) b: Galactic Latitude (deg)
(4) d: Distance (pc)
(5) RV_LSR: Radial Velocity in the LSR frame (km/s)
(6) U: U motion along the Heliocentric Galactic Cartesian x direction (km/s)
(7) V: V motion along the Heliocentric Galactic Cartesian y direction (km/s)
(8) W: W motion along the Heliocentric Galactic Cartesian z direction (km/s)
(9) U_LSR : U motion along the Heliocentric Galactic Cartesian x direction in the LSR frame (km/s)
(10) V_LSR : V motion along the Heliocentric Galactic Cartesian y direction in the LSR frame (km/s)
(11) W_LSR : W motion along the Heliocentric Galactic Cartesian z direction in the LSR frame (km/s)
(12) X: Heliocentric Galactic Cartesian x position (pc)
(13) Y: Heliocentric Galactic Cartesian y position (pc)
(14) Z: Heliocentric Galactic Cartesian z position (pc)<br
Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat
No full textThe involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemic conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.LR: 20061115; PUBM: Print; JID: 0372763; 0 (Gastrointestinal Hormones); 11061-68-0 (Insulin); 59392-49-3 (Gastric Inhibitory Polypeptide); ppublishSource type: Electronic(1
Low-carbohydrate diets affect energy balance and fuel homeostasis differentially in lean and obese rats
No full textIn parallel with increased prevalence of overweight people in affluent societies are individuals trying to lose weight, often using low-carbohydrate diets. Nevertheless, long-term metabolic consequences of those diets, usually high in (saturated) fat, remain unclear. Therefore, we investigated long-term effects of high-fat diets with different carbohydrate/protein ratios on energy balance and fuel homeostasis in obese (fa/fa) Zucker and lean Wistar rats. Animals were fed high-carbohydrate (HC), high-fat (HsF), or low-carbohydrate, high-fat, high-protein (LC-HsF-HP) diets for 60 days. Both lines fed the LC-HsF-HP diet displayed reduced energy intake compared with those fed the HsF diet (Zucker, -3.7%) or the HC diet (Wistar rats, -12.4%). This was not associated with lower weight gain relative to HC fed rats, because of increased food efficiencies in each line fed HsF and particularly LC-HsF-HP food. Zucker rats were less glucose tolerant than Wistar rats. Lowest glucose tolerances were found in HsF and particularly in LC-HsF-HP-fed animals irrespective of line, but this paralleled reduced plasma adiponectin levels, elevated plasma resistin levels, higher retroperitoneal fat masses, and reduced insulin sensitivity (indexed by insulin-induced hypoglycemia) only in Wistar rats. In Zucker rats, however, improved insulin responses during glucose tolerance testing and tendency toward increased insulin sensitivities were observed with HsF or LC-HsF-HP feeding relative to HC feeding. Thus, despite adverse consequences of LC-HsF diets on blood glucose homeostasis, principal differences exist in the underlying hormonal regulatory mechanisms, which could have benefits for B-cell functioning and insulin action in the obese state but not in the lean state.
3D Cloud Skeletons
No full textFits tables containing the (x,y,z,l,b,d) coordinates of the points defining each cloud's skeleton. We include results for both the "longest path" skeleton, and the full, unpruned skeleton. The heliocentric cartesian coordinates ( x,y,z ) are provided in parsecs. The plane of the sky coordinates, Galactic Longitude (l ) and Galactic Latitude (b ) are provided in degrees. The distance d is provided in parsecs
Glucokinase activity in isolated islets from obese fa/fa Zucker rats
No full textGlucokinase (EC 2.7.1.2) activity of B-cells was measured in extracted pancreatic islets isolated from lean and obese fa/fa Zucker rats and maintained in primary culture overnight. Formation of [14C]glucose phosphoric esters from D-[U-14C]glucose was measured in the presence of unlabelled glucose from 0.05 to 0.50 mM for hexokinase (EC 2.7.1.1) activity, and 8.0-16.0 mM unlabelled glucose for glucokinase activity. Eadie-Hofstee analysis revealed that hexokinase kinetic parameters (Vmax and Km) for [14C]glucose phosphoric ester formation were similar in lean- and fa/fa-rat islets. For glucokinase, there was no difference in Vmax. between phenotypes. A non-significant tendency to increased sensitivity to glucose was noted in the fa/fa-rat islets (P = 0.13). In lean-rat islets, the glucokinase inhibitor mannoheptulose (3 mM) decreased Vmax. by 80% and increased the apparent Km from 3.3 +/- 0.7 mM to 12.2 +/- 2.0 mM (P < 0.05). There was no difference in Km or Vmax. in mannoheptulose-treated versus control islets from fa/fa rats. This lack of effect was consistent with reported effects of mannoheptulose on insulin secretion from fa/fa-rat islets [Chan, MacPhail and Mitton (1993) Can. J. Physiol. Pharmacol. 71, 34-39]. The data from glucose and mannoheptulose experiments support the hypothesis that glucokinase function is altered in fa/fa Zucker rats and may contribute to fasting hyperinsulinaemia in vivo in these animals.LR: 20061115; PUBM: Print; JID: 2984726R; 11061-68-0 (Insulin); 654-29-5 (Mannoheptulose); EC 2.7.1.1 (Hexokinase); EC 2.7.1.2 (Glucokinase); ppublishSource type: Electronic(1
Evaluation of the zucker diabetic fatty (ZDF) rat as a model for human disease based on urinary peptidomic profiles
No full textRepresentative animal models for diabetes-associated vascular complications are extremely relevant in assessing potential therapeutic drugs. While several rodent models for type 2 diabetes (T2D) are available, their relevance in recapitulating renal and cardiovascular features of diabetes in man is not entirely clear. Here we evaluate at the molecular level the similarity between Zucker diabetic fatty (ZDF) rats, as a model of T2D-associated vascular complications, and human disease by urinary proteome analysis. Urine analysis of ZDF rats at early and late stages of disease compared to age- matched LEAN rats identified 180 peptides as potentially associated with diabetes complications. Overlaps with human chronic kidney disease (CKD) and cardiovascular disease (CVD) biomarkers were observed, corresponding to proteins marking kidney damage (eg albumin, alpha-1 antitrypsin) or related to disease development (collagen). Concordance in regulation of these peptides in rats versus humans was more pronounced in the CVD compared to the CKD panels. In addition, disease-associated predicted protease activities in ZDF rats showed higher similarities to the predicted activities in human CVD. Based on urinary peptidomic analysis, the ZDF rat model displays similarity to human CVD but might not be the most appropriate model to display human CKD on a molecular level
Evidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′
No full textFirst evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Measurement of the B0–B0 oscillation frequency Δmd with the decays B0→D−π+ and B0→ J/ψK∗0
No full textThe B
0
–B
0
oscillation frequency Δmd is measured by the LHCb experiment using a dataset corresponding
to an integrated luminosity of 1.0 fb−1
of proton–proton collisions at √
s = 7 TeV, and is found to be
Δmd
=0.5156±0.0051 (stat.)±0.0033 (syst.) ps−1
. The measurement is based on results from analyses
of the decays B
0
→ D
−π
+ (D
−
→ K
+π
−π
−) and B
0
→ J/ψK
∗0
(J/ψ →μ
+μ
−,K
∗0
→ K
+π
−) and
their charge conjugated modes
Altered CCK induced satiety in obese Zucker rats.
No full text<p>A) Obese Zucker rats weigh significantly more than lean Zucker rats (N = 12; t-test). B) Immunoblot of pSTAT3 in VAN of lean (top) and obese (bottom) Zucker rats treated with vehicle or leptin. C) Densitometry analysis of <i>B</i> showing that STAT3 is phosphorylated in response to leptin (i.p) in VAN of lean Zucker rats but not in obese Zucker rats. N = 4 D) Immunoblot of pSTAT3 in hypothalamus of lean and obese Zucker rats treated with leptin. E) Densitometry analysis of <i>D</i> showing that STAT3 is phosphorylated in response to leptin in the arcuate nucleus of the hypothalamus of lean Zucker rats, but not obese Zucker rats. (N = 4).F) CCK8S (i.p., 0.22 nmol/kg) significantly inhibited food intake in lean Zucker rats but not obese Zucker rats. N = 6. Data expressed as mean ± SEM. Significant differences were represented as <sup>a,b,c</sup> between groups in one-way ANOVA. Significant differences were represented as * for p<0.05; ** for p<0.01; and *** for p<0.001 in Student's t-test.</p
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