bluuebunny/crossref_metadata_2025_split huggingface dataset:
What Determines Nutritional Recovery in Malnourished Children After Correction of Congenital Heart Defects?
Authors: Vaidyanathan Balu , Radhakrishnan Reshma , Sarala Deepa Aravindakshan , Sundaram Karimassery Ramaiyar , Kumar Raman Krishna 
Published: July 2009

BACKGROUND: Malnutrition is common in children with congenital heart disease (CHD), especially in developing countries.
OBJECTIVE: To examine the impact of corrective intervention on the nutritional status of children with CHD and identify factors associated with suboptimal recovery.
METHODS: Consecutive patients with CHD in a tertiary center in South India were evaluated for nutritional status before and 2 years after corrective intervention. Anthropometry was performed at presentation and every 6 months for 2 years, and z scores were compared. Malnutrition was defined as a weight-for-age, height-for-age, and weight/height z score &lt;−2. Determinants of malnutrition were entered into a multivariate logistic regression analysis model.
RESULTS: Of 476 patients undergoing corrective intervention (surgical: 344; catheter-based: 132) z scores of less than −2 for weight for age, height for age, and weight/height were recorded in 59%, 26.3%, and 55.9% of patients, respectively, at presentation. On follow-up (425 patients [92.5% of survivors; 20.63 ± 13.1 months of age]), z scores for weight for age and weight/height improved significantly from the baseline (weight: −1.42 ± 1.03 vs −2.19 ± 1.16; P &lt; .001; weight/height: −1.15 ± 1.25 vs −2.09 ± 1.3; P &lt; .001). Height-for-age z scores were not significantly different. Malnutrition persisted in 116 (27.3%) patients on follow-up and was associated with a birth weight of ≤2.5 kg, nutritional status at presentation, and height of parents and not with type of cardiac lesion, dietary intake, or socioeconomic factors.
CONCLUSIONS: This study from South India demonstrates severe malnutrition in over half of the patients with CHD and is not always reversed by corrective surgery or intervention. Persistent malnutrition after corrective intervention is predicted by nutritional status at presentation, birth weight, and parental anthropometry.
Serum α-Fetoprotein Response as a Surrogate for Clinical Outcome in Patients Receiving Systemic Therapy for Advanced Hepatocellular Carcinoma
Authors: Vora Sadhna R. , Zheng Hui , Stadler Zsofia K. , Fuchs Charles S. , Zhu Andrew X. 
Published: July 2009

Abstract

Background.
The role of serum α-fetoprotein (AFP) as a marker for treatment response in patients with hepatocellular carcinoma (HCC) receiving systemic therapy is poorly defined.

Methods.
A retrospective study was performed on patients with advanced HCC enrolled in five phase II clinical trials. Serum AFP was prospectively collected at baseline and at different time points through treatment in parallel with radiologic response and clinical outcome. Patients were separated into three groups based on a 50% change in serum AFP from baseline. Overall survival (OS), progression-free survival (PFS), and radiologic responses were compared between groups using log-rank and Wilcoxon tests.

Results.
Of 144 patients, 107 met the eligibility criteria. Eighteen patients experienced a &gt;50% AFP decline, 57 patients had a &gt;50% AFP increase, and 32 patients had a &lt;50% change in serum AFP in either direction. Compared with patients with a &lt;50% change in serum AFP (median PFS, 5.6 months), patients with a &gt;50% AFP decrease had a longer PFS time (median, 16.9 months; p = .029), whereas those with a &gt;50% increase had a shorter PFS time (median, 2.3 months; p = .038). Patients with a &gt;50% rise in AFP had a shorter OS time than those with a &lt;50% change (median, 6.3 months versus 11.1 months, respectively; p = .004), whereas a &gt;50% AFP decrease was not associated with a significant difference in OS (median, 13.0 months; p = .87). AFP changes were significantly associated with radiologic response.

Conclusions.
Our study suggests that serum AFP change during treatment may serve as a useful surrogate marker for clinical outcome in patients with advanced HCC receiving systemic therapy.
Studying Genetic Variations in Cancer Prognosis (and Risk): A Primer for Clinicians
Authors: Savas Sevtap , Liu Geoffrey 
Published: July 2009

Learning ObjectivesEvaluate SNPs as genetic markers and functional genetic variations. Select candidate genes for cancer research based on knowledge of their biological function. Assess candidate gene and genome-wide association studies for their potential to improve translational research.This article is available for continuing medical education credit at CME.TheOncologist.com
Chemical diversity in Brassica oleracea affects biodiversity of insect herbivores
Authors: Poelman Erik H. , Dam Nicole Mvan , Loon Joop J. Avan , Vet Louise E. M. , Dicke Marcel 
Published: July 2009

Intraspecific variation in plants plays a major role in the composition and diversity of the associated insect community. Resistance traits of plants are likely candidates mediating community composition. However, it is debated whether total concentrations of chemical compounds or specific compounds determine herbivore resistance, and how chemical diversity among plant genotypes in turn affects the composition of the associated herbivore community.To study the role of specific chemical compounds in affecting the herbivore community, we used cultivated Brassica oleracea. The cultivars differ qualitatively in glucosinolate profile, i.e., foliar composition of different glucosinolate compounds, and only a little in total concentration of glucosinolates, the secondary metabolites specific for the Brassicaceae family. In field and laboratory experiments, we tested whether individual compounds explained differences in herbivore community composition, and whether herbivores with a similar degree of host plant specialization responded in a similar way to variation in glucosinolate profiles.In the field B. oleracea cultivars differed widely in species richness and composition of the herbivore community, as well as in the density of insects they harbored. Plants with high concentrations of the short side chain alkenyl glucosinolate, glucoiberin, harbored low herbivore diversity. Higher biodiversity was found when plants had glucosinolate profiles containing high concentrations of glucosinolates with elongated side chains, which are biosynthetically linked to glucoiberin. Although glucosinolates are known to have differential effects on generalist and specialist herbivores, all herbivore species exhibited similar responses to the intraspecific variation in foliar glucosinolate profiles of the B. oleracea cultivars. This observation is supported by the correspondence between oviposition preferences of the specialist herbivore Pieris rapae and the generalist Mamestra brassicae in the field and the laboratory, using the same cultivars, and may be due to the relatively low concentrations of glucosinolates in cultivars. Our results show that variation in the concentration of short side‐chain glucosinolates affects the composition of the herbivore community associated with brassicaceous plants.
Fluid Flow in a Fractured Reservoir Using a Geomechanically Constrained Fault-Zone-Damage Model for Reservoir Simulation
Authors: Paul Pijush , Zoback Mark , Hennings Peter 
Published: July 2009

SummarySecondary fractures and faults associated with reservoir-scale faults affect both permeability and permeability anisotropy and hence play an important role in controlling the production behavior of a faulted reservoir. It is well known from geologic studies that there is a concentration of secondary fractures and faults in damage zones adjacent to large faults. Because there are usually inadequate data to fully incorporate damage-zone fractures and faults into reservoir-simulation models, this study uses the principles of dynamic rupture propagation from earthquake seismology to predict the nature of fractured/damage zones associated with reservoir-scale faults. We include geomechanical constraints in our reservoir model and propose a generalized workflow to incorporate damage zones into reservoir-simulation models more routinely.The model we propose calculates the extent of the damage zone along the fault plane by estimating the volume of rock brought to failure by the stress perturbation associated with dynamic-rupture propagation. We apply this method to a real reservoir using both field- and well-scale observations. At the rupture front, damage intensity gradually decreases as we move away from the rupture front or fault plane. In the studied reservoir, the secondary-failure planes in the damage zone are high-angle normal faults striking subparallel to the parent fault, which may affect the permeability of the reservoir in both horizontal and vertical directions. We calibrate our modeling with both outcrop and well observations from a number of studies. We show that dynamic-rupture propagation gives a reasonable first-order approximation of damage zones in terms of permeability and permeability anisotropy in order to be incorporated into reservoir simulators.
Systemic Fate of the Adipocyte-Derived Factor Adiponectin
Authors: Halberg Nils , Schraw Todd D. , Wang Zhao V. , Kim Ja-Young , Yi James , Hamilton Mark P. , Luby-Phelps Kate , Scherer Philipp E. 
Published: July 2009

OBJECTIVE
The adipocyte-derived secretory protein adiponectin has been widely studied and shown to have potent insulin-sensitizing, antiapoptotic, and anti-inflammatory properties. While its biosynthesis is well understood, its fate, once in circulation, is less well established.

RESEARCH DESIGN AND METHODS
Here, we examine the half-life of adiponectin in circulation by tracking fluorescently labeled recombinant adiponectin in the circulation, following it to its final destination in the hepatocyte.

RESULTS
Despite its abundant presence in plasma, adiponectin is cleared rapidly with a half-life of ∼75 min. A more bioactive version carrying a mutation at cysteine 39 is cleared within minutes. Even though steady-state levels of adiponectin differ between male and female mice, we failed to detect any differences in clearance rates, suggesting that differences in plasma are mostly due to differential production rates. In a metabolically challenged state (high-fat diet exposure or in an ob/ob background), adiponectin levels are reduced in plasma and clearance is significantly prolonged, reflecting a dramatic drop in adiponectin production levels.

CONCLUSIONS
Combined, these results show a surprisingly rapid turnover of adiponectin with multiple fat pads contributing to the plasma levels of adiponectin and clearance mediated primarily by the liver. It is surprising that despite high-level production and rapid clearance, plasma levels of adiponectin remain remarkably constant.
Prediction of Metabolic Syndrome by Low Serum Testosterone Levels in Men
Authors: Haring Robin , Völzke Henry , Felix Stephan B. , Schipf Sabine , Dörr Marcus , Rosskopf Dieter , Nauck Matthias , Schöfl Christof , Wallaschofski Henri 
Published: July 2009

OBJECTIVE
The aim of this analysis was to assess the prospective association of serum testosterone and dehydroepiandrosterone sulfate (DHEAS) levels with incident metabolic syndrome (MetS) in men.

RESEARCH DESIGN AND METHODS
Data were obtained from the Study of Health in Pomerania (SHIP), a population-based prospective cohort of adults aged 20–79 years. Analyses were conducted in 1,004 men without baseline MetS defined by National Cholesterol Education Program Adult Treatment Panel III guidelines. Testosterone and DHEAS were categorized by age-specific quartiles and Poisson regression models with relative risks (RRs) and 95% CIs were estimated.

RESULTS
After a median follow-up time of 5.0 years, 480 men (47.8%) developed MetS. Testosterone levels decreased with increasing number of MetS components. Testosterone in the lowest quartile predicted MetS (RR 1.38 [95% CI 1.13–1.69]), particularly among men aged 20–39 years (2.06 [1.29–3.29]), even after adjustment for age, smoking, alcohol consumption, physical activity, waist circumference, self-related health, and time of blood sampling. DHEAS levels were not related to incident MetS (0.99 [0.83–1.19]).

CONCLUSIONS
Low testosterone but not DHEAS predicts development of MetS in a population-based cohort of 1,004 men aged 20–79 years. Especially in young men aged 20–39 years, results suggest low testosterone as a strong predictor for incident MetS. Assessment of testosterone in young and middle-age men may allow early interventions in the general population.
Enhanced Hypothalamic Glucose Sensing in Obesity: Alteration of Redox Signaling
Authors: Colombani Anne-Laure , Carneiro Lionel , Benani Alexandre , Galinier Anne , Jaillard Tristan , Duparc Thibaut , Offer Géraldine , Lorsignol Anne , Magnan Christophe , Casteilla Louis , Pénicaud Luc , Leloup Corinne 
Published: July 2009

OBJECTIVE
Recent data demonstrated that glucose sensing in different tissues is initiated by an intracellular redox signaling pathway in physiological conditions. However, the relevance of such a mechanism in metabolic disease is not known. The aim of the present study was to determine whether brain glucose hypersensitivity present in obese Zücker rats is related to an alteration in redox signaling.

RESEARCH DESIGN AND METHODS
Brain glucose sensing alteration was investigated in vivo through the evaluation of electrical activity in arcuate nucleus, changes in reactive oxygen species levels, and hypothalamic glucose-induced insulin secretion. In basal conditions, modifications of redox state and mitochondrial functions were assessed through oxidized glutathione, glutathione peroxidase, manganese superoxide dismutase, aconitase activities, and mitochondrial respiration.

RESULTS
Hypothalamic hypersensitivity to glucose was characterized by enhanced electrical activity of the arcuate nucleus and increased insulin secretion at a low glucose concentration, which does not produce such an effect in normal rats. It was associated with 1) increased reactive oxygen species levels in response to this low glucose load, 2) constitutive oxidized environment coupled with lower antioxidant enzyme activity at both the cellular and mitochondrial level, and 3) overexpression of several mitochondrial subunits of the respiratory chain coupled with a global dysfunction in mitochondrial activity. Moreover, pharmacological restoration of the glutathione hypothalamic redox state by reduced glutathione infusion in the third ventricle fully reversed the cerebral hypersensitivity to glucose.

CONCLUSIONS
The data demonstrated that obese Zücker rats' impaired hypothalamic regulation in terms of glucose sensing is linked to an abnormal redox signaling, which originates from mitochondria dysfunction.
The C3a Anaphylatoxin Receptor Is a Key Mediator of Insulin Resistance and Functions by Modulating Adipose Tissue Macrophage Infiltration and Activation
Authors: Mamane Yaël , Chung Chan Chi , Lavallee Genevieve , Morin Nicolas , Xu Li-Jing , Huang JingQi , Gordon Robert , Thomas Winston , Lamb John , Schadt Eric E. , Kennedy Brian P. , Mancini Joseph A. 
Published: July 2009

OBJECTIVESignificant new data suggest that metabolic disorders such as diabetes, obesity, and atherosclerosis all posses an important inflammatory component. Infiltrating macrophages contribute to both tissue-specific and systemic inflammation, which promotes insulin resistance. The complement cascade is involved in the inflammatory cascade initiated by the innate and adaptive immune response. A mouse genomic F2 cross biology was performed and identified several causal genes linked to type 2 diabetes, including the complement pathway.RESEARCH DESIGN AND METHODSWe therefore sought to investigate the effect of a C3a receptor (C3aR) deletion on insulin resistance, obesity, and macrophage function utilizing both the normal-diet (ND) and a diet-induced obesity mouse model.RESULTSWe demonstrate that high C3aR expression is found in white adipose tissue and increases upon high-fat diet (HFD) feeding. Both adipocytes and macrophages within the white adipose tissue express significant amounts of C3aR. C3aR−/− mice on HFD are transiently resistant to diet-induced obesity during an 8-week period. Metabolic profiling suggests that they are also protected from HFD-induced insulin resistance and liver steatosis. C3aR−/− mice had improved insulin sensitivity on both ND and HFD as seen by an insulin tolerance test and an oral glucose tolerance test. Adipose tissue analysis revealed a striking decrease in macrophage infiltration with a concomitant reduction in both tissue and plasma proinflammatory cytokine production. Furthermore, C3aR−/− macrophages polarized to the M1 phenotype showed a considerable decrease in proinflammatory mediators.CONCLUSIONSOverall, our results suggest that the C3aR in macrophages, and potentially adipocytes, plays an important role in adipose tissue homeostasis and insulin resistance.
Antinuclear Antibody and Rheumatoid Factor in Silica-Exposed Workers
Authors: Aminian Omid , Sharifian Seyed , Mehrdad Ramin , Haghighi Khosro , Mazaheri Maria 
Published: July 2009

Antinuclear Antibody and Rheumatoid Factor in Silica-Exposed WorkersA lot of workers in industries such as foundry, stonecutting, and sandblasting are exposed to higher than permissible levels of crystalline silica. Various alterations in humoral immune function have been reported in silicosis patients and workers exposed to silica dust. The aim of this study was to measure antinuclear antibody (ANA) and rheumatoid factor (RF) levels in foundry workers exposed to silica and to compare them with a control group without such exposure. ANA and RF were measured in 78 exposed and 73 non-exposed workers, and standard statistical methods were used to compare them. The two groups did not significantly differ in age and smoking. Mean work duration of the exposed and non-exposed workers was (14.9±4.72) years and (12.41±6.3) years, respectively. Ten exposed workers had silicosis. ANA was negative in all workers in either group. Its mean titer did not differ significantly between the exposed and control workers [(0.39±0.15) IU mL-1vs. (0.36±0.17) IU mL-1, respectively]. RF was positive in two workers of each group. Other studies have reported an increase in ANA and RF associated with exposure to silica dust and silicosis.In contrast, our study suggests that exposure to silica dust does not increase the level of ANA and RF in exposed workers.
Radioprotective Effects of Quercetin and Ethanolic Extract of Propolis in Gamma-Irradiated Mice
Authors: Benković Vesna , Knežević Anica , Đikić Domagoj , Lisičić Duje , Oršolić Nada , Bašić Ivan , Kopjar Nevenka 
Published: July 2009

Radioprotective Effects of Quercetin and Ethanolic Extract of Propolis in Gamma-Irradiated MiceThe aim of this study was to assess radioprotective effects of quercetin and the ethanolic extract of propolis (EEP) in CBA mice exposed to a single radiation dose 4 Gy (60Co). The mice were treated with 100 mg kg-1quercetin or EEP a day for three consecutive days either before (pre-treatment) or after gamma-irradiation (therapy). Leukocyte count was determined in blood drawn from the tail vein, and DNA damage in leukocytes was assessed using the alkaline comet assay. Genotoxic effects of the test compunds were also evaluated in non-irradiated mice. The levels of radioprotection provided by both test compounds were compared with those established in mice that were given chemical radioprotector S-(2-Aminoethy1)isothiouronium bromide hydrobromide (AET). Mice that received pre-treatment were less sensitive to irradiation. Mice given the post-irradiation therapy showed a slight but not significant increase in total leukocyte count over irradiated negative control. Quercetin showed better protective properties than EEP in both pre-treatment and therapy, and activated a higher number of leukocytes in non-irradiated mice. The alkaline comet assay suggests that both natural compounds, especially when given as pre-treatment, protect against primary leukocyte DNA damage in mice. At tested concentrations, EEP and quercetin were not genotoxic to non-irradiated mice. AET, however, caused a slight but not significant increase in DNA damage. Although the results of this study show the radioprotective potential of the test compounds, further investigation is needed to clarify the underlying protection mechanisms.
D-Amphetamine Toxicity in Freshly Isolated Rat Hepatocytes: A Possible Role of CYP3A
Authors: Vitcheva Vessela , Kondeva-Burdina Magdalena , Mitcheva Mitka 
Published: July 2009

D-Amphetamine Toxicity in Freshly Isolated Rat Hepatocytes: A Possible Role of CYP3AThe aim of this study was to trace D-amphetamine toxicity in isolated rat hepatocytes and to elucidate a possible involvement of CYP3A in the mechanisms of its toxicity. To this end, male Wistar rats were treated with nifedipine (5 mg kg-1i.p., 5 days), a substrate and inducer of CYP3A. Hepatocytes isolated from nifedipine-treated and control rats were incubated with D-amphetamine at a concentration of 100 μmol L-1, which was determined to be an average toxic concentration (TC50) for the compound. To evaluate the possible toxic effects of D-amphetamine on freshly isolated rat hepatocytes, we assessed the following parameters: cell viability, lactate dehydrogenase (LDH) activity, and glutathione (GSH).The results showed that nifedipine potentiated amphetamine cytotoxicityin vitro, as follows: cell viability dropped by 65% (p>0.001), GSH by 80% (p>0.001), and LDH activity increased by 190% (p>0.001). To clarify the role of nifedipine in amphetamine cytotoxicity, we used amiodarone, a substrate and an inhibitor of CYP3A. Pre-incubation of nifedipine-treated hepatocytes with amiodarone (14 μmol L-1) significantly lowered amphetamine cytotoxicity.Our results confirmed the toxicity of D-amphetamine in isolated rat hepatocytes and the involvement of CYP3A in its metabolism and hepatotoxicity.
Comparative Effects of Calcium Channel Blockers, Autonomic Nervous System Blockers, and Free Radical Scavengers On Diazinon-Induced Hyposecretion Of Insulin From Isolated Islets of Langerhans in Rats
Authors: Pourkhalili Nazila , Pournourmohammadi Shirin , Rahimi Fatemeh , Vosough-Ghanbari Sanaz , Baeeri Maryam , Ostad Seyed , Abdollahi Mohammad 
Published: July 2009

Comparative Effects of Calcium Channel Blockers, Autonomic Nervous System Blockers, and Free Radical Scavengers On Diazinon-Induced Hyposecretion Of Insulin From Isolated Islets of Langerhans in RatsHyperglycaemia has been observed with exposure to organophosphate insecticides. This study was designed to compare the effects of calcium channel blockers, alpha-adrenergic, beta-adrenergic, and muscarinic receptor blockers, and of free radical scavengers on insulin secretion from diazinon-treated islets of Langerhans isolated from the pancreas of rats using standard collagenase digestion, separation by centrifugation, and hand-picking technique. The islets were then cultured in an incubator at 37 °C and 5 % CO2. In each experimental set 1 mL of 8 mmol L-1glucose plus 125 μg mL-1or 625 μg mL-1of diazinon were added, except for the control group, which received 8 mmol L-1glucose alone. The cultures were then treated with one of the following: 30 μmol L-1atropine, 100 μmol L-1ACh + 10 μmol L-1neostigmine, 0.1 μmol L-1propranolol, 2 μmol L-1nifedipine, 50 μmol L-1phenoxybenzamine, or 10 μmol L-1alphatocopherol. In all experiments, diazinon significantly reduced glucose-stimulated insulin secretion at both doses, showing no dose dependency, as the average inhibition for the lower dose was 62.20 % and for the higher dose 64.38 %. Acetylcholine and alpha-tocopherol restored, whereas atropine potentiated diazinon-induced hyposecretion of insulin. Alpha-, beta- and calcium channel blockers did not change diazinon-induced effects. These findings suggest that diazinon affects insulin secretion mainly by disturbing the balance between free radicals and antioxidants in the islets of Langerhans and by inducing toxic stress.