bluuebunny/crossref_metadata_2025_split huggingface dataset:
Application of Tripodal Linker Units to Immobilized Rhodium Complex Catalysts for Asymmetric Hydrogenation
Authors: Fukaya Norihisa , Onozawa Shun-ya , Ueda Masae , Miyaji Takayuki , Takagi Yukio , Sakakura Toshiyasu , Yasuda Hiroyuki 
Published: January 2011

Abstract
The tripodal linker unit with one bromopropyl group and three anchoring silicon atoms was used to immobilize a chiral phosphine–rhodium complex catalyst on an ordered mesoporous silica support. The rhodium and phosphorus leaching levels into the reaction solution after asymmetric hydrogenation were lower for this catalyst than for immobilized catalysts prepared using conventional triethoxysilane.
Preparation and Intercalation Properties of Novel Layered Zinc 1,3,5-Benzenetriphosphonates Composed of Anionic Hybrid Layers
Authors: Maeda Kazuyuki , Hatasawa Haruna , Kawawa Kanako , Nagayoshi Naoko , Matsushima Yuta 
Published: January 2011

Abstract
Zinc 1,3,5-benzenetriphosphonates (ZBP) prepared in the presence of organic cations contain unique layers composed of inorganic 1D chains bridged with benzene rings. ZBP showed intercalation and cation-exchange properties while retaining the layer structure, resembling layered metal phosphates rather than conventional layered phosphonates.
What is the best predictor of the atherogenic LDL subclass phenotype ‘pattern B’ in patients with type 2 diabetes mellitus?
Authors: King R I , Florkowski C M , Yeo J , Walmsley T A , Shand B I , Scott R S , George P M 
Published: January 2011

Background The atherogenic lipoprotein phenotype ‘pattern B’ comprises a predominance of small-dense low-density lipoprotein (sdLDL). Gradient gel electrophoresis (GGE) is considered a ‘gold standard’ method for identifying this phenotype, but is impractical for routine laboratory use. The low-density lipoprotein cholesterol:apolipoprotein-B (LDL-C:Apo-B) ratio has been advocated as a surrogate marker for sdLDL and a direct assay for sdLDL has recently become available. We compared the sdLDL assay and LDL-C:Apo-B with more established lipid parameters to predict the presence of ‘pattern B’ phenotype. Method Blood was collected from 97 fasted subjects on three separate occasions. Total cholesterol, triglyceride, Apo-B and sdLDL were measured; LDL- and HDL-cholesterol were determined after ultracentrifugation. The predominant LDL particle size and phenotype were assigned by GGE. Results ‘Pattern B’ phenotype was identified in 36% of samples. Peak particle size showed a positive correlation with HDL-cholesterol and a negative correlation with triglyceride and Apo-B. Receiver operating curve (ROC) analysis showed triglyceride:HDL-C ratio and triglyceride alone to be the best predictors of ‘pattern B’ phenotype, with area under the curve (AUC) being 0.87 and 0.84, respectively. AUCs for sdLDL (0.74) and LDL-C:Apo-B (0.71) were significantly lower ( P < 0.05). A high sdLDL concentration had the greatest specificity (95%) and positive predictive value (74%) for ‘pattern B’ phenotype, but low sensitivity (43%). Conclusion Direct measurement of sdLDL provided the most specific predictor of ‘pattern B’ phenotype, whereas triglyceride:HDL-C ratio or triglycerides alone, parameters readily available in most laboratories, were the best predictors by ROC analysis.
New Plant Venture Performance Differences Among Incumbent, Diversifying, and Entrepreneurial Firms: The Impact of Industry Learning Intensity
Authors: Balasubramanian Natarajan 
Published: January 2011

Prior firm experience, firm capabilities, and the industry environment are known to be important determinants of new-venture performance. We hypothesize that firm experience prior to setting up a new venture influences the ability to learn from experience after start-up (which is a key capability), and that this relationship is moderated by the importance of learning by doing within the new venture's industry (which is a critical aspect of the industry environment). We argue that together, these relationships influence performance differences among new plant ventures of incumbents, diversifying entrants, and entrepreneurial (de novo) entrants. Using data on 47,915 new plant ventures in U.S. manufacturing, we find that incumbents and diversifying entrants establish significantly more productive new plants than de novo entrants, and that this advantage significantly increases with the importance of learning by doing in an industry (industry learning intensity). These productivity differences appear to be driven more by learning subsequent to plant start-up than by initial disparities in productivity. Together, these findings strongly suggest that pre-start-up experience adds to the process of post-start-up learning, and that the industry learning environment plays an important role in whether entrepreneurial firms can achieve a competitive advantage over existing firms.This paper was accepted by Lee Fleming, entrepreneurship.
Ab Initio Electron Diffraction Structure Analysis of Zeolites – Direct Methods Determination of NaY
Authors: Dorset Douglas L. , Gilmore Christopher J. 
Published: January 2011

Abstract
The crystal structure of NaY was re-determined in space group Fd-3m from 87 unique electron diffraction amplitudes obtained at 1250 kV by A. Carlsson, et al. (Chem. Eur. J. 5 (1999) 244), where a = 24.7 Å. The determination, based on maximum entropy and likelihood (computer program MICE), leads to a clearly resolved structure, in contrast to the use of crystallographic phases derived from the Fourier transforms of experimental high-resolution images cited in the above paper. Potential maps from a trial solution contain density sites that correspond closely to the known T-site locations of this FAU framework. Although only framework T-site positions and not linkage oxygens are observed in the map, they can be linked with theoretical oxygens. Subsequent distance least squares (DLS) refinement of the linked model converges to a complete framework structure very close to the one found in earlier X-ray diffraction studies. Contrasting to the earlier study, where no counterion positions were identified, two possible Na positions were clearly visible in the direct phasing map One of these corresponds to a site postulated in previous studies. The other is near a site proposed in a separate electron microscopic/electron diffraction study of Na,FeY. Least squares refinement verifies the former position while eliminating the latter. On the other hand, a separate direct analysis of a dataset from the Y zeolite containing both Na and Fe (Carlsson et al., loc. cit.) was not successful, owing to the smaller number of recorded amplitudes.
Income Distribution, Search and Market Efficiency
Authors: Simhon Avi , Fishman Arthur 
Published: January 2011

Abstract
This paper explores the relationship between income distribution, prices, production efficiency and aggregate output in a decentralized search economy. We show that income distribution determines how competitive prices are and thereby affects production efficiency and aggregate output. It is shown that, under reasonable assumptions, it is possible to engineer a judicious transfer of income from high to low income individuals, which increases income equality, leads to more competitive prices, and increases aggregate output.
The Expression and Function of Glucose-Dependent Insulinotropic Polypeptide in the Embryonic Mouse Pancreas
Authors: Prasadan Krishna , Koizumi Masayuki , Tulachan Sidhartha , Shiota Chiyo , Lath Nikesh , Paredes Jose , Guo Ping , El-Gohary Yousef , Malek Marcus , Shah Sohail , Gittes George K. 
Published: January 2011

OBJECTIVE
Glucose-dependent insulinotropic polypeptide (GIP) is a member of a structurally related group of hormones that also includes glucagon, glucagon-like peptides, and secretin. GIP is an incretin, known to modulate glucose-induced insulin secretion. Recent studies have shown that glucagon is necessary for early insulin-positive differentiation, and a similar role for incretins in regulating embryonic insulin-positive differentiation seems probable. Here we studied the role of GIP signaling in insulin-positive differentiation in the embryonic mouse pancreas.

RESEARCH DESIGN AND METHODS
The ontogeny of the GIP ligand and GIP receptor in the embryonic pancreas was investigated by immunohistochemistry and RT-PCR. GIP signaling was inhibited in cultured embryonic pancreata using morpholine-ring antisense against GIP ligand and receptor, or small interfering RNA (siRNA) for GIP ligand and receptor. Markers of endocrine cells and their progenitors were studied by immunohistochemistry and RT-PCR.

RESULTS
GIP and GIP receptor mRNA were both detected in the embryonic pancreas by embryonic day 9.5 and then persisted throughout gestation. GIP was generally coexpressed with glucagon by immunostaining. The GIP receptor was typically coexpressed with insulin. Morpholine-ring antisense or siRNA against either GIP ligand or GIP receptor both inhibited the differentiation of insulin-positive cells. Inhibition of GIP or its receptor also led to a decrease in the number of Pdx-1–positive and sox9-positive cells in the cultured embryonic pancreas. The number of Pax6- and Nkx2.2-positive cells, representative of developing pancreatic endocrine cells and β-cells, respectively, was also decreased.

CONCLUSIONS
GIP signaling may play a role in early embryonic pancreas differentiation to form insulin-positive cells or β-cells.
A Newly Identified CG301269 Improves Lipid and Glucose Metabolism Without Body Weight Gain Through Activation of Peroxisome Proliferator–Activated Receptor α and γ
Authors: Jeong Hyun Woo , Lee Joo-Won , Kim Woo Sik , Choe Sung Sik , Kim Kyung-Hee , Park Ho Seon , Shin Hyun Jung , Lee Gha Young , Shin Dongkyu , Lee Hanjae , Lee Jun Hee , Choi Eun Bok , Lee Hyeon Kyu , Chung Heekyoung , Park Seung Bum , Park Kyong Soo , Kim Hyo-Soo , Ro Seonggu , Kim Jae Bum 
Published: January 2011

OBJECTIVE
Peroxisome proliferator–activated receptor (PPAR)-α/γ dual agonists have been developed to alleviate metabolic disorders. However, several PPARα/γ dual agonists are accompanied with unwanted side effects, including body weight gain, edema, and tissue failure. This study investigated the effects of a novel PPARα/γ dual agonist, CG301269, on metabolic disorders both in vitro and in vivo.

RESEARCH DESIGN AND METHODS
Function of CG301269 as a PPARα/γ dual agonist was assessed in vitro by luciferase reporter assay, mammalian one-hybrid assay, and analyses of PPAR target genes. In vitro profiles on fatty acid oxidation and inflammatory responses were acquired by fatty acid oxidation assay and quantitative (q)RT-PCR of proinflammatory genes. In vivo effect of CG301269 was examined in db/db mice. Total body weight and various tissue weights were measured, and hepatic lipid profiles were analyzed. Systemic glucose and insulin tolerance were measured, and the in vivo effect of CG301269 on metabolic genes and proinflammatory genes was examined by qRT-PCR.

RESULTS
CG301269 selectively stimulated the transcriptional activities of PPARα and PPARγ. CG301269 enhanced fatty acid oxidation in vitro and ameliorated insulin resistance and hyperlipidemia in vivo. In db/db mice, CG301269 reduced inflammatory responses and fatty liver, without body weight gain.

CONCLUSIONS
We demonstrate that CG301269 exhibits beneficial effects on glucose and lipid metabolism by simultaneous activation of both PPARα and PPARγ. Our data suggest that CG301269 would be a potential lead compound against obesity and related metabolic disorders.
Reduction in Basal Nitric Oxide Activity Causes Albuminuria
Authors: Ott Christian , Schneider Markus P. , Delles Christian , Schlaich Markus P. , Schmieder Roland E. 
Published: January 2011

OBJECTIVE
The barrier function of the glomerular filter has been studied for decades. Albuminuria reflects a malfunction of this barrier, and in animals dysfunctional endothelial nitric-oxide (NO) synthase results in albuminuria. We aimed to analyze the importance of NO for the glomerular barrier function in humans.

RESEARCH DESIGN AND METHODS
To assess the effect of endothelial dysfunction on albuminuria, we measured the urine albumin-to-creatinine ratio (UACR) both before and after the blockade of NO synthases (NOSs) with systemic infusion of NG-monomethyl-l-arginine (l-NMMA) in two distinct study populations. In population A, 62 hypertensive patients with type 2 diabetes and, in population B, 22 patients with hypercholesterolemia but without hypertension or type 2 diabetes were examined. All subjects had normal renal function.

RESULTS
There was a significant increase in the UACR in response to NOS inhibition with l-NMMA in hypertensive patients with type 2 diabetes (study population A) and in patients with hypercholesterolemia (study population B). Linear regression analyses revealed that the change in mean arterial presssure in response to l-NMMA was not related to the increase in the UACR in response to l-NMMA in either population, even after adjusting for filtration fraction.

CONCLUSIONS
NOS inhibition provokes albuminuria that is unrelated to changes in blood pressure. It is noteworthy that this finding was evident in patient groups prone to endothelial dysfunction and albuminuria. Thus, acute deterioration of endothelial function by reducing NO activity causes an increase in albuminuria.
The Same Chromosome 9p21.3 Locus Is Associated With Type 2 Diabetes and Coronary Artery Disease in a Chinese Han Population
Authors: Cheng Xiang , Shi Lisong , Nie Shaofang , Wang Fan , Li Xiuchun , Xu Chengqi , Wang Pengyun , Yang Baofeng , Li Qingxian , Pan Zhenwei , Li Yue , Xia Hao , Zheng Chenhong , Ke Yuhe , Wu Yanxia , Tang Tingting , Yan Xinxin , Yang Yan , Xia Ni , Yao Rui , Wang Binbin , Ma Xu , Zeng Qiutang , Tu Xin , Liao Yuhua , Wang Qing K. 
Published: January 2011

OBJECTIVE
Recent genome-wide association studies (GWAS) revealed that a 9p21.3 locus was associated with type 2 diabetes. In this study, we carried out a large-scale case-control study in the GeneID Chinese Han population to 1) further replicate the association of 9p21.3 type 2 diabetes GWAS single nucleotide polymorphisms (SNPs) and 2) assess the association of these SNPs with coronary artery disease.

RESEARCH DESIGN AND METHODS
Three SNPs (rs2383208, rs10811661, and rs10757283) were genotyped in two GeneID cohorts of 3,167 Chinese Han individuals. Case-control association design was used to determine the association of the SNPs with type 2 diabetes and coronary artery disease. Gensini scores were calculated in the coronary artery disease subjects and were tested for association with the variants. Multivariate logistic regressions were performed on association studies.

RESULTS
The association between two of the three SNPs and type 2 diabetes was replicated in the GeneID population (rs2383208, P = 0.936; rs10811661-T, P = 0.02, odds ratio [OR] = 1.23; rs10757283-C, P = 0.003, OR = 1.30). The same two SNPs also contributed to the risk of coronary artery disease (CAD) (rs10811661-T, P = 0.002, OR = 1.19; rs10757283-C, P = 0.003, OR = 1.18). In addition, rs10757283 was associated with severity of coronary atherosclerosis estimated by the Gensini scoring system (risk allele C, quantitative-trait regression adjusted P = 0.002).

CONCLUSIONS
For the first time to our knowledge, our results indicated that the same 9p21.3 locus, represented by SNPs rs10811661 and rs10757283, contributed to the risk of type 2 diabetes and coronary artery disease in our GeneID Chinese Han population.
Hyperglycemia Activates Caspase-1 and TXNIP-Mediated IL-1β Transcription in Human Adipose Tissue
Authors: Koenen Tim B. , Stienstra Rinke , van Tits Lambertus J. , de Graaf Jacqueline , Stalenhoef Anton F.H. , Joosten Leo A.B. , Tack Cees J. , Netea Mihai G. 
Published: January 2011

OBJECTIVEObesity is characterized by elevated levels of proinflammatory cytokines, including interleukin (IL)-1β, that contribute to the development of insulin resistance. In this study, we set out to investigate whether hyperglycemia drives IL-1β production and caspase-1 activation in murine and human adipose tissue, thus inducing insulin resistance.RESEARCH DESIGN AND METHODSob/ob animals were used as a model to study obesity and hyperglycemia. Human adipose tissue fragments or adipocytes were cultured in medium containing normal or high glucose levels. Additionally, the role of thioredoxin interacting protein (TXNIP) in glucose-induced IL-1β production was assessed.RESULTSTXNIP and caspase-1 protein levels were more abundantly expressed in adipose tissue of hyperglycemic ob/ob animals as compared with wild-type mice. In human adipose tissue, high glucose resulted in a 10-fold upregulation of TXNIP gene expression levels (P &lt; 0.01) and a 10% elevation of caspase-1 activity (P &lt; 0.05), together with induction of IL-1β transcription (twofold, P &lt; 0.01) and a significant increase in IL-1β secretion. TXNIP suppression in human adipocytes, either by a small interfering RNA approach or a peroxisome proliferator–activated receptor-γ agonist, counteracted the effects of high glucose on bioactive IL-1 production (P &lt; 0.01) mainly through a decrease in transcription levels paralleled by reduced intracellular pro-IL-1β levels.CONCLUSIONSHigh glucose activates caspase-1 in human and murine adipose tissue. Glucose-induced activation of TXNIP mediates IL-1β mRNA expression levels and intracellular pro-IL-1β accumulation in adipose tissue. The concerted actions lead to enhanced secretion of IL-1β in adipose tissue that may contribute to the development of insulin resistance.
Progression of Carotid Artery Intima-Media Thickness During 12 Years in the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study
Authors: Polak Joseph F. , Backlund Jye-Yu C. , Cleary Patricia A. , Harrington Anita P. , O’Leary Daniel H. , Lachin John M. , Nathan David M. ,   for the DCCT/EDIC Research Group
Published: January 2011

OBJECTIVE
This study investigated the long-term effects of intensive diabetic treatment on the progression of atherosclerosis, measured as common carotid artery intima-media thickness (IMT).

RESEARCH DESIGN AND METHODS
A total of 1,116 participants (52% men) in the Epidemiology of Diabetes Interventions and Complications (EDIC) trial, a long-term follow-up of the Diabetes Control and Complications Trial (DCCT), had carotid IMT measurements at EDIC years 1, 6, and 12. Mean age was 46 years, with diabetes duration of 24.5 years at EDIC year 12. Differences in IMT progression between DCCT intensive and conventional treatment groups were examined, controlling for clinical characteristics, IMT reader, and imaging device.

RESULTS
Common carotid IMT progression from EDIC years 1 to 6 was 0.019 mm less in intensive than in conventional (P &lt; 0.0001), and from years 1 to 12 was 0.014 mm less (P = 0.048); but change from years 6 to 12 was similar (intensive − conventional = 0.005 mm, P = 0.379). Mean A1C levels during DCCT and DCCT/EDIC were strongly associated with progression of IMT, explaining most of the differences in IMT progression between DCCT treatment groups. Albuminuria, older age, male sex, smoking, and higher systolic blood pressure were significant predictors of IMT progression.

CONCLUSIONS
Intensive treatment slowed IMT progression for 6 years after the end of DCCT but did not affect IMT progression thereafter (6–12 years). A beneficial effect of prior intensive treatment was still evident 13 years after DCCT ended. These differences were attenuated but not negated after adjusting for blood pressure. These results support the early initiation and continued maintenance of intensive diabetes management in type 1 diabetes to retard atherosclerosis.
Selective Reversible Inhibition of Liver Carnitine Palmitoyl-Transferase 1 by Teglicar Reduces Gluconeogenesis and Improves Glucose Homeostasis
Authors: Conti Roberto , Mannucci Edoardo , Pessotto Pompeo , Tassoni Emanuela , Carminati Paolo , Giannessi Fabio , Arduini Arduino 
Published: January 2011

OBJECTIVE
We have developed a new antihyperglycemic agent (teglicar) through the selective and reversible inhibition of the liver isoform of carnitine palmitoyl-transferase 1 (L-CPT1).

RESEARCH DESIGN AND METHODS
Glucose production was investigated in isolated hepatocytes and during pancreatic clamps in healthy rats. Chronic treatments on C57BL/6J, db/db, high-fat fed mice, and rats were performed to understand glucose metabolism and insulin sensitivity.

RESULTS
In isolated hepatocytes, teglicar concentration dependently reduced ketone bodies and glucose production up to 72 and 50%, respectively. In rats, teglicar reduced the endogenous glucose production (−62%) without affecting peripheral glucose utilization. Heart 2-[3H]deoxyglucose uptake in mice was also not affected, confirming in vivo the drug selectivity toward L-CPT1. Chronic treatment in db/db mice (50 mg/kg/bid; 45 days) reduced postabsorptive glycemia (−38%), water consumption (−31%), and fructosamine (−30%). Such antidiabetic activity was associated with an improved insulin sensitivity assessed by the insulin tolerance test. A significant 50% increase in hepatic triglyceride content (HTGC) was found, although plasma alanineaminotransferase was not altered. In addition, long-term teglicar administration to high-fat fed C57BL/6J mice normalized glycemia (−19%) and insulinemia (−53%). Long-term teglicar administration (30 days, 80 mg/kg) in healthy overnight-fasted rats slightly reduced basal glycemia (−20%, ns), reduced basal insulin levels by 60%, doubled triglycerides, and increased free-fatty acids (+53%). HTGC was markedly increased, but liver and peripheral insulin sensitivity assessed by hyperinsulinemiceuglycemic clamp were not affected.

CONCLUSIONS
Teglicar, in vitro and in animal models, reduces gluconeogenesis and improves glucose homeostasis, refreshing the interest in selective and reversible L-CPT1 inhibition as a potential antihyperglycemic approach.
Participation of Hindbrain AMP-Activated Protein Kinase in Glucoprivic Feeding
Authors: Li Ai-Jun , Wang Qing , Ritter Sue 
Published: January 2011

OBJECTIVE
To examine the role of AMP-activated protein kinase (AMPK) in the control of glucoprivic feeding by hindbrain catecholamine neurons.

RESEARCH DESIGN AND METHODS
Micropunched hindbrain samples were collected from control and 2-deoxy-d-glucose (2DG)-injected rats for Western blot analysis of phosphorylated (activated) AMPK (pAMPK). Samples also were collected from 2DG-injected rats pretreated with anti-dopamine-β-hydroxylase conjugated to saporin to lesion hindbrain catecholamine neurons. In a second experiment, rats were given a fourth-ventricle injection of compound C (CC) or 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR), an inhibitor and activator of AMPK, to identify a role for AMPK in hindbrain neurons required for elicitation of 2DG-induced feeding.

RESULTS
Systemic 2DG stimulated food intake in controls but not in catecholamine-lesioned rats. In controls, but not catecholamine-lesioned rats, 2DG also increased phosphorylated Thr172 at AMPKα subunits (pAMPKα) in hindbrain micropunches containing catecholaminergic cell groups A1 through the middle region of C1 (A1–C1m). Increased pAMPKα was not observed in the adjacent noncatecholaminergic ventromedial medulla or in the A2–C2 catecholamine cell groups in the dorsal hindbrain. Fourth-ventricle injection of CC attenuated 2DG-induced feeding during the first 2 h of the test, and AICAR alone increased food intake only during the first 60 min of the 4-h test.

CONCLUSIONS
Results indicate that AMPK in catecholaminergic A1–C1m neurons is activated by glucoprivation. Therefore, AMPK may contribute to the glucose-sensing mechanism by which these neurons detect and signal a glucose deficit in the service of systemic glucoregulation.