bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q10
Authors: Lim S. C. , Tan H. H. , Goh S. K. , Subramaniam T. , Sum C. F. , Tan I. K. , Lee B. L. , Ong C. N. 
Published: November 2006

AbstractAim  Individuals with diabetes and prediabetes are at risk of vascular injury. However, the exact mechanisms are unclear. The mitochondria mobile electron carrier coenzyme Q10 (CoQ10) is a potent lipophilic antioxidant. We hypothesize that oxidative stress, detectable as changes in plasma CoQ10 concentrations and composition, plays an important role in vascular disease in diabetes.Methods  We measured plasma CoQ10 concentrations (including reduced ubiquinol and oxidized ubiquinone subfractions) in 60 subjects with normal glucose tolerance [NGT; fasting plasma glucose (FPG) < 5.5 mmol/l], 63 with impaired fasting glucose (IFG; FPG 5.6–6.9 mmol/l) and 69 with Type 2 diabetes (DM; FPG > 6.9 mmol/l).Results  In men and women, the total CoQ10/total cholesterol ratio was reduced in DM (mean ±sd) [male (M) 0.09 ± 0.04; female (F) 0.07 ± 0.04] compared with NGT (0.29 ± 0.08; 0.21 ± 0.07) and IFG (0.27 ± 0.07; 0.23 ± 0.07) (DM vs. NGT and IFG P = 0.001). A stepwise reduction in the plasma ubiquinol fraction (ubiquinol/total CoQ10) was observed from NGT (M 0.93 ± 0.06; F 0.95 ± 0.06) compared with IFG (0.43 ± 0.25; 0.41 ± 0.15) and DM (0.24 ± 0.11; F 0.29 ± 0.16) (DM vs. IFG vs. NGT P = 0.001). In contrast, the plasma ubiquinone/ubiquinol ratio increased from NGT (M 0.08 ± 0.07, F 0.06 ± 0.08) to IFG (2.14 ± 1.84, 1.75 ± 1.04) to DM (4.77 ± 4.88, 3.81 ± 3.71) (DM vs. IFG vs. NGT P = 0.001). These differences remained after adjusting for age, body mass index and FPG.Conclusions  The change in CoQ10 with increasing FPG concentration suggests an increase in oxidative burden, already evident in the prediabetic IFG individuals. This increase in oxidative stress might contribute to the increased risk of vascular disease.
Cortisol—cause and cure for metabolic syndrome?
Authors: Walker B. R. 
Published: November 2006

AbstractSimilarities between the metabolic syndrome and Cushing's syndrome, and reversibility of the features of Cushing's syndrome, suggest that cortisol may contribute to the pathophysiology of both conditions and that reducing cortisol action may provide a novel therapeutic approach in the metabolic syndrome. There is substantial evidence that circulating cortisol concentrations are higher in people with hypertension and glucose intolerance. The basis for this activation of the hypothalamic–pituitary–adrenal axis remains uncertain, but it may be attributable to ‘programming’ effects of events in early life, since it is associated with low birth weight. In obese people, intracellular cortisol levels within adipose tissue are further amplified by increased local regeneration of cortisol by the enzyme 11β‐HSD type 1. In mice, transgenic manipulations of 11β‐HSD1 have potent effects on obesity and associated features of the metabolic syndrome. Promising preclinical data suggest that novel 11β‐HSD1 inhibitors will have a role in lowering intracellular cortisol levels as a treatment for the metabolic syndrome. In addition to their metabolic effects, glucocorticoids act in the blood vessel wall. Pharmacoepidemiological studies suggest that glucocorticoid excess is an independent risk factor for cardiovascular disease. Recent data suggest that 11β‐HSD1 within the blood vessel wall influences vascular remodelling and angiogenesis, for example in the myocardium following coronary artery occlusion. Thus, glucocorticoid signalling provides a potentially tractable system to influence both risk factors for, and the outcome of, Type 2 diabetes and cardiovascular disease.
Hepatocyte nuclear factor‐1 beta mutations cause neonatal diabetes and intrauterine growth retardation: support for a critical role of HNF‐1β in human pancreatic development
Authors: Edghill E. L. , Bingham C. , Slingerland A. S. , Minton J. A. L. , Noordam C. , Ellard S. , Hattersley A. T. 
Published: November 2006

AbstractAim  The transcription factor hepatocyte nuclear factor‐1beta (HNF‐1β) is expressed in rodent pancreatic progenitor cells, where it is an important member of the genetic hierarchy that regulates the generation of pancreatic endocrine and exocrine cells. The recent description of an HNF‐1β mutation in a patient with neonatal diabetes suggests that HNF‐1β may also play a key role in human pancreatic B‐cell development. We aimed to investigate the role of HNF‐1β mutations in neonatal diabetes and also the impact of HNF‐1β mutations on fetal growth.Methods  We sequenced the HNF‐1β gene in 27 patients with neonatal diabetes in whom other known genetic aetiologies had been excluded. Birth weight was investigated in 21 patients with HNF‐1β mutations.Results  A heterozygous HNF‐1β mutation, S148L, was identified in one patient with neonatal diabetes diagnosed at 17 days, which rapidly resolved only to relapse at 8 years. This patient had pancreatic atrophy, mild exocrine insufficiency and low birth weight (1.83 kg at 40 weeks’ gestation). Intrauterine growth was markedly reduced in patients born to unaffected mothers with a median birth weight of 2.4 kg (range 1.8–3.3) (P = 0.006), median centile weight 3 (0.008–38), and 69% were small for gestational age.Conclusion  HNF‐1β mutations are a rare cause of neonatal diabetes as well as pancreatic exocrine and endocrine dysfunction. Low birth weight is a common feature of patients with HNF‐1β mutations and is consistent with reduced insulin secretion in utero. These findings support a key role for HNF‐1β in early pancreatic progenitor cells in man.
Peroxisome proliferator‐activated receptor (PPAR) delta genetic polymorphism and its association with insulin resistance index and fasting plasma glucose concentrations in Chinese subjects
Authors: Hu C. , Jia W. , Fang Q. , Zhang R. , Wang C. , Lu J. , Xiang K. 
Published: November 2006

AbstractAims  Previous studies have shown that the peroxisome proliferator‐activated receptor delta (PPARD) genetic polymorphism affects cholesterol metabolism in Whites. This association was not observed in a Korean population in a separate study, but this study showed a link between the PPARD polymorphism and body weight and fasting plasma glucose. The purpose of this study was to determine whether polymorphisms of PPARD influence glucose and cholesterol metabolism in Chinese subjects. We investigated the association between the polymorphism (−87T/C) of the human PPARD gene and phenotypes related to body weight, insulin sensitivity, glucose and lipid metabolism in Chinese subjects.Methods  Unrelated Chinese subjects (n = 663) in Shanghai were studied; 287 had newly diagnosed Type 2 diabetes mellitus and 376 were non‐diabetic control subjects over 40 years old. Clinical parameters were collected and genotypes were determined by polymerase chain reaction‐restriction fragment length polymorphism.Results  In normal glucose tolerant (NGT) subjects, the C allele carriers had higher fasting plasma glucose concentrations (P = 0.0078) and a lower insulin sensitivity index (ISI) (P = 0.0365). The C allele carriers also showed higher concentrations of low‐density lipoprotein cholesterol (P = 0.0261) and percentage of body fat (P = 0.0357). There was a trend towards higher visceral adiposity in C allele carriers, but the difference was not significant (P = 0.0830). In diabetes patients, similar results were detected for plasma glucose concentrations (fasting plasma glucose P < 0.0001, 2‐h plasma glucose P = 0.0052) and insulin sensitivity (homeostasis model assessment of insulin resistance P = 0.0094; ISI P = 0.0058).Conclusion  The PPARD−87T/C polymorphism is associated with higher fasting plasma glucose concentrations in both NGT and diabetic subjects, largely due to impaired insulin sensitivity.
Prevalence of and risk factors for extracranial internal carotid artery stenosis in Korean Type 2 diabetic patients
Authors: Park J. H. , Kim W. H. , Kim J. H. , Park T. S. , Baek H. S. 
Published: November 2006

AbstractAims  The objectives of this study were to evaluate the prevalence of and risk factors for extracranial internal carotid artery stenosis in Type 2 diabetic patients.Methods  This study included 406 patients aged 40–79 years with Type 2 diabetes (male 55.4%, female 44.6%). Both carotid arteries of each patient were examined by carotid duplex scanning. The duplex ultrasound criteria based on the North American Symptomatic Carotid Endarterectomy Trial (NASCET) measurement method were used for the identification of carotid stenosis.Results  Extracranial internal carotid artery stenosis ≥ 40% by velocity criteria was detected in 5.2% of the patients. The prevalence of carotid stenosis increased with advancing age: 1.0% at 40–49 years of age, 5.0% at 50–59 years, 7.3% at 60–69 years and 9.5% at 70–79 years. The degree of stenosis was > 70% in 42.9% of patients with stenosis, Bilateral stenosis was detected in 14% of patients. Of the patients with ≥ 40% carotid stenosis, 33% had a decreased ankle‐brachial index, 38% had a previous history of stroke, and only one patient (5%) had a documented history of coronary artery disease. Multivariate analysis, including variables determined to be significantly different by univariate analysis between patients with or without ≥ 40% stenosis, indicated that age, systolic blood pressure and high‐density lipoprotein (HDL)‐cholesterol (inverse correlation) were independent risk factors associated with carotid stenosis.Conclusions  Carotid duplex scanning is a useful strategy in identifying carotid stenosis in older Type 2 diabetic patients with high systolic blood pressure, or low levels of HDL cholesterol. The early identification and subsequent appropriate management of carotid stenosis, particularly in this group of patients, may facilitate efforts to reduce the incidence of macrovascular complications.
Engineering of a sialic acid synthesis pathway in transgenic plants by expression of bacterial Neu5Ac‐synthesizing enzymes
Authors: Paccalet Thomas , Bardor Muriel , Rihouey Christophe , Delmas Frédéric , Chevalier Christian , D’Aoust Marc‐André , Faye Loïc , Vézina Louis , Gomord Véronique , Lerouge Patrice 
Published: November 2006

SummaryPlants are a low‐cost and contamination‐free factory for the production of recombinant pharmaceutical proteins. However, plant‐made pharmaceuticals differ from their mammalian homologues by the structure of their N‐linked glycans. For instance, most mammalian glycoproteins harbour terminal sialic acids that control their half‐life in the bloodstream. The absence of the whole sialylation machinery in plants is of major concern as non‐sialylated plant‐made pharmaceuticals may not perform at their full potential in humans, because of their removal from the circulation through the involvement of hepatic cell receptors. In this context, we have investigated the synthesis of N‐acetylneuraminic acid (Neu5Ac) in the cytosol of plants by either the re‐routing of the endogenous 3‐deoxy‐d‐manno‐2‐octulosonic acid (Kdo) biosynthetic pathway or the expression of microbial Neu5Ac‐synthesizing enzymes. In this paper, we demonstrate that the plant Kdo‐8P synthase is not able to use N‐acetyl d‐mannosamine as a substrate, and thus re‐routing of the Kdo pathway for the synthesis of Neu5Ac is not possible. Consequently, we expressed genes encoding Neu5Ac lyase from Escherichia coli and Neu5Ac synthase (neuB2) from Campylobacter jejuni in plants. These resulted in the production of functional enzymes in the cytosol, which in turn can catalyse the synthesis of Neu5Ac in vitro. Experiments were carried out on two models, Bright Yellow 2 (BY2) tobacco cells and Medicago sativa (alfalfa), the perennial legume crop.
Eleven microsatellite loci isolated from the banded wren (Thryothorus pleurostictus)
Authors: BRAR R. K. , SCHOENLE L. A. , STENZLER L. M. , HALL M. L. , VEHRENCAMP S. L. , LOVETTE I. J. 
Published: November 2006

AbstractWe describe 11 microsatellite loci isolated from the banded wren (Thryothorus pleurostictus), a Neotropical species for which understanding the genetic mating system is important for testing questions about the species’ unusual vocal behaviour. Screening of these loci revealed extremely low allelic variation in a Costa Rican population. Allelic variation at these and other previously developed loci is substantially higher in two other wren species, the southern house wren (Troglodytes aedon bonariae) and rufous‐and‐white wren (Thryothorus rufalbus), suggesting that the low allelic diversity in the banded wren results from demographic bottlenecks rather than locus‐sampling artefacts.
Isolation of polymorphic microsatellite loci from Eurasian woodcock (Scolopax rusticola) and their cross‐utility in related species
Authors: CARDIA P. , FERRERO M. E. , GONÇALVES D. , DÁVILA J. A. , FERRAND N. 
Published: November 2006

AbstractWe isolated one trinucleotide and seven tetranucleotide microsatellite loci for the Eurasian woodcock (Scolopax rusticola). We describe polymerase chain reaction conditions and primers for the successful amplification of these loci and report the results obtained from their use in 42 specimens from two populations in Europe. The number of alleles per locus ranged from three to 15, observed heterozygosity was comprised between 0.11 and 1.00 and expected heterozygosity ranged between 0.10 and 0.91. Cross‐specific amplification experiments highlighted the potential usefulness of these molecular markers for the study of three related scolopacid waders.
Development of 19 microsatellite loci for Swainson's hawks (Buteo swainsoni) and other buteos
Authors: HULL JOSHUA M. , TUFTS DANIELLE , TOPINKA J. RICK , MAY BERNIE , ERNEST HOLLY B. 
Published: November 2006

AbstractWe developed 26 Swainson's hawk (Buteo swainsoni) microsatellite primers from CA, AAT, CATC and GAGAA enriched genomic libraries. Primers were tested in 357 Swainson's hawks from western North America as well as seven other Buteo species. These markers will have broad application in investigations of Buteo population structure and genetic diversity.
Incorporating spatial autocorrelation may invert observed patterns
Authors: Kühn Ingolf 
Published: November 2006

ABSTRACTThough still often neglected, spatial autocorrelation can be a serious issue in ecology because the presence of spatial autocorrelation may alter the parameter estimates and error probabilities of linear models. Here I re‐analysed data from a previous study on the relationship between plant species richness and environmental correlates in Germany. While there was a positive relationship between native plant species richness and an altitudinal gradient when ignoring the presence of spatial autocorrelation, the use of a spatial simultaneous liner error model revealed a negative relationship. This most dramatic effect where the observed pattern was inverted may be explained by the environmental situation in Germany. There the highest altitudes are in the south and the lowlands in the north that result in some locally or regionally inverted patterns of the large‐scale environmental gradients from the equator to the north. This study therefore shows the necessity to consider spatial autocorrelation in spatial analyses.
Seasonal reversals of upland‐riparian diversity gradients in the Sonoran Desert
Authors: Stromberg J. C. 
Published: November 2006

ABSTRACTFlood disturbance and water resource availability vary sharply over time and space along arid‐region rivers and can interact in complex fashion to shape diversity patterns. Plant diversity showed spatial patterning along a topogradient from the floodplain of the San Pedro River (Arizona, USA) to the arid upland, but the patterns shifted temporally as the suite of limiting factors changed. During two of three sampling times, spatial diversity patterns were shaped primarily by gradients of water availability, the regional limiting factor. In the summer dry season, microscale diversity (species richness per 1 m2) and mesoscale diversity (cumulative species and functional types in 20, 1‐m2 plots) of herbaceous plants decreased along the topogradient from floodplain to upland, reflecting the greater water availability on the low surfaces. During a summer wet season with moderate rains and flooding, diversity increased in all hydrogeomorphic zones (floodplain, terrace, upland), but the spatial pattern along the topogradient persisted. Following a very wet winter, patterns along the topogradient reversed: scour from large floods limited diversity on the floodplain and competitive exclusion limited the diversity on undisturbed river terrace, while abundant rains allowed for high microscale diversity in the upland. Disturbance and resource availability thus interacted to influence plant species diversity in a fashion consistent with the dynamic‐equilibrium model of species diversity. In contrast to the microscale patterns, mesoscale diversity of species and functional types remained high in the floodplain during all sampling times, with 58% more plant species and 90% more functional types sampled in low floodplain than arid upland for the year as a whole. Species with a wide range of moisture and temperature affinities were present in the floodplain, and seasonal turnover of species was high in this zone. The floodplain zone of a perennial to intermittent‐flow river thus had greater plant diversity than arid Sonoran Desert upland, as measured at temporal scales that capture seasonal variance in resource and disturbance pulses and at spatial scales that capture the environmental heterogeneity of floodplains. Although periodically limited by intense flood disturbance, diversity remains high in the floodplain because of the combination of moderate resource levels (groundwater, seasonal flood water) and persistent effects of flood disturbance (high spatial heterogeneity, absence of competitive exclusion), in concert with the same climatic factors that produce seasonally high diversity in the region (temporally variable pulses of rainfall).
Cyanobacterial calcification, carbon dioxide concentrating mechanisms, and Proterozoic–Cambrian changes in atmospheric composition
Authors: RIDING R. 
Published: November 2006

ABSTRACTPhotosynthetic uptake of inorganic carbon can raise the pH adjacent to cyanobacterial cells, promoting CaCO3 precipitation. This effect is enhanced by CO2 concentrating mechanisms that actively transport into cells for carbon fixation. CO2 concentrating mechanisms presumably developed in response to atmospheric decrease in CO2 and increase in O2 over geological timescales. In present‐day cyanobacteria, CO2 concentrating mechanisms are induced when the atmospheric partial pressure of CO2 (pCO2) falls below ∼0.4%. Reduction in pCO2 during the Proterozoic may have had two successive effects on cyanobacterial calcification. First, fall in pCO2 below ∼1% (33 times present atmospheric level, PAL) resulted in lower dissolved inorganic carbon (DIC) concentrations that reduced pH buffering sufficiently for isolated CaCO3 crystals to begin to nucleate adjacent to cyanobacterial cells. As a result, blooms of planktic cyanobacteria induced precipitated ‘whitings’ of carbonate mud in the water column whose sedimentary accumulation began to dominate carbonate platforms ∼1400–1300 Ma. Second, fall in pCO2 below ∼0.4% (10 PAL) induced CO2‐concentrating mechanisms that further increased pH rise adjacent to cells and promoted in vivo cyanobacterial sheath calcification. Crossing of this second threshold is indicated in the fossil record by the appearance of Girvanella 750–700 Ma. Coeval acquisition of CO2 concentrating mechanisms by planktic cyanobacteria further stimulated whiting production. These inferences, that pCO2 fell below ∼1%∼1400–1300 Ma and below ∼0.4% 750–700 Ma, are consistent with empirical and modelled palaeo‐atmosphere estimates. Development of CO2 concentrating mechanisms was probably temporarily slowed by global cooling ∼700–570 Ma that favoured diffusive entry of CO2 into cells. Lower levels of temperature and DIC at this time would have reduced seawater carbonate saturation state, also hindering cyanobacterial calcification. It is suggested that as Earth emerged from ‘Snowball’ glaciations in the late Neoproterozoic, global warming and O2 rise reactivated the development of CO2 concentrating mechanisms. At the same time, rising levels of temperature, calcium ions and DIC increased seawater carbonate saturation state, stimulating widespread cyanobacterial in vivo sheath calcification in the Early Cambrian. This biocalcification event promoted rapid widespread development of calcified cyanobacterial reefs and transformed benthic microbial carbonate fabrics.
A Survey of Neurologists on Self‐treatment and Treatment of Their Families
Authors: Evans Randolph W. , Lipton Richard B. , Ritz Kristin A. 
Published: November 2006

Background.—Although neurologists commonly self‐treat for migraine and other conditions, little is known about the patterns of self‐treatment by physicians in the United States.Objectives.—The aim was to obtain information about neurologist's self‐treatment and treatment of family members and their attitudes about self‐treatment by other physicians.Methods.—A survey was performed among neurologists attending the Texas Neurological Society's Winter Conference using a questionnaire about self‐treatment and treatment of family members during the prior 12 months and attitudes about self‐treatment by other physicians.Results.—Among 186 physicians invited to participate, the response rate was 48%. Although 76% reported having primary care physicians, neurologists reported the following behaviors: 38% self‐diagnosed or self‐treated medical conditions including migraine in 25%; 56% started themselves on prescription medications including 21% who used triptans and 15% who used migraine preventive medications; 33% ordered blood tests on themselves; and 20% ordered imaging studies on themselves. Sixty percent reported missing no work due to illness, 87% missed 2 days or less, and 99% reported missing 1 week or less. Eighty percent reported treating their family members for acute minor illnesses and 33% for chronic conditions. The following percentage of participants reported that they would be likely to self‐diagnose and self‐treat the following hypothetical illnesses: 70%, migraines which were not severe; 19%, new onset frequent headaches; and 48%, chronic daily headaches. The following percentage of participants agreed or strongly agreed that the following behaviors were acceptable for physicians: 94%, self‐treat acute minor illnesses; 37%, self‐treat chronic conditions; 42%, order blood test for diagnostic purposes; 40%, order imaging studies for diagnostic purposes; 87%, treat family members for acute minor conditions; and 36%, treat family members for chronic conditions.Conclusions.—Neurologists commonly treat themselves and family members.